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                    <title><![CDATA[Endometrial Cancer]]></title>

                    <link>https://www.benthamscience.com</link>

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                    RSS Feed for Disease Wise Article | BenthamScience

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                    <pubDate>Sat, 06 Jun 2026 22:39:58 +0000</pubDate>

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                    <title><![CDATA[Endometrial Cancer]]></title>

                    <url>https://www.benthamscience.com</url>

                    <link>https://www.benthamscience.com</link>

                    </image><item><title><![CDATA[E2F1 Reduces Sorafenib’s Sensitivity of Esophageal Carcinoma Cells via
Modulating the miR-29c-3p/COL11A1 Signaling Axis]]></title><link>https://www.benthamscience.comarticle/130004</link><description><![CDATA[<P>Objective: Esophageal carcinoma (ESCA) is a common malignancy characterized by high morbidity and mortality. Our work managed to dissect the modulatory mechanism of E2F1/miR-29c-3p/COL11A1 in the malignant progression and sensitivity of ESCA cells to sorafenib. <P> Methods: Via bioinformatics approaches, we identified the target miRNA. Subsequently, CCK-8, cell cycle analysis, and flow cytometry were used to check the biological influences of miR-29c-3p on ESCA cells. TransmiR, mirDIP, miRPathDB, and miRDB databases were used as tools for the prediction of upstream transcription factors and downstream genes of miR-29c-3p. The targeting relationship of genes was detected via RNA immunoprecipitation and chromatin immunoprecipitation, which was further validated by dual-luciferase assay. Finally, in vitro experiments revealed the way E2F1/miR-29c-3p/COL11A1 affected sorafenib’s sensitivity, and in vivo experiments were used to verify the way E2F1 and sorafenib impacted ESCA tumor growth. <P> Results: miR-29c-3p, downregulated in ESCA, could suppress ESCA cell viability, arrest the cell cycle in the G0/G1 phase, and impel apoptosis. E2F1 was found to be upregulated in ESCA and it could abate the transcriptional activity of miR-29c-3p. COL11A1 was found to be a downstream target of miR-29c-3p to enhance cell viability, induce cell cycle arrest in S phase, and constrain apoptosis. Cellular and animal experiments together demonstrated that E2F1 abated the sorafenib’s sensitivity of ESCA cells via miR-29c-3p/COL11A1. <P> Conclusion: E2F1 affected the viability, cell cycle, and apoptosis of ESCA cells by modulating miR-29c-3p/COL11A1, and it attenuated the sensitivity of ESCA cells to sorafenib, shedding new light on the treatment of ESCA.</P>]]></description> </item><item><title><![CDATA[Mammalian Target of Rapamycin (mTOR) Signalling Pathway-A Potential
Target for Cancer Intervention: A Short Overview]]></title><link>https://www.benthamscience.comarticle/130571</link><description><![CDATA[<p>Background: The mammalian role of the rapamycin (mTOR) pathway is the practical nutrient-sensitive regulation of animal growth and plays a central role in physiology, metabolism, and common diseases. The mTOR is activated in response to nutrients, growth factors, and cellular energy. The mTOR pathway activates in various cellular processes and human cancer diseases. Dysfunction of mTOR signal transduction is associated with metabolic disorders, cancer for instance. <p> Objective: In recent years, significant achievements envisaged in developing targeted drugs for cancer. The global impact of cancer continues to grow. However, the focus of disease-modifying therapies remains elusive. The mTOR is a significant target in cancer to be considered for mTOR inhibitors, even though the costs are high. Despite many mTOR inhibitors, potent, selective inhibitors for mTOR are still limited. Therefore, in this review, the mTOR structure and protein-ligand interactions of utmost importance to provide the basis for molecular modelling and structure-based drug design are discussed. <p> Conclusion: This review introduces the mTOR, its crystal structure, and the latest research on mTOR.Besides, the role of mTOR in cancer, its function, and its regulation are reviewed. In addition, the mechanistic role of mTOR signalling networks in cancer and interaction with drugs that inhibit the development of mTOR and crystal structures of mTOR and its complexes are explored. Finally, the current status and prospects of mTOR-targeted therapy are addressed.</p>]]></description> </item><item><title><![CDATA[IMPDH2 Positively Impacts the Proliferation Potential of Hepatoblastoma Cells
by Activating JunB Signaling Pathway]]></title><link>https://www.benthamscience.comarticle/138645</link><description><![CDATA[<P>Background: Amplification of inosine monophosphate dehydrogenase II, EC 1,1,1,205 (IMPDH2) has been reported in various cancers, which results in transformation and tumorigenicity. In our current work, we have explored the oncogenic properties and the underlying pathophysiology of IMPDH2 in hepatoblastoma (HB). <P> Methods: To investigate IMPDH2 expression in HB tissues and prognostic significance in HB patients, gene expression profiling interactive analysis (GEPIA) has been adopted. Immunohistochemistry has also helped to validate the protein expression of IMPDH2 in HB tissues. The effect of IMPDH2 overexpression or depletion on the proliferation of Hepatoblastoma cells in vitro has been evaluated by CCK8 assays and colony formation assays. Xenograft tumor growth of mice has been detected. Luciferase reporter assays have been conducted to determine the interaction of IMPDH2 and JunB, which was further asserted by pharmacological inhibition of JunB. <P> Results: IMPDH2 was highly expressed in HB tissues. Experimentally, the proliferation and colony formation of HuH6 cells were increased by IMPDH2 overexpression. Conversely, genetic inactivation of IMPDH2 impaired the proliferative efficiency and colony-forming rate of HepG2 cells. Besides, the luciferase reporter assay validated IMPDH2 overexpression to be associated with enhanced JunB transcriptional activity, while its activity was diminished in the case of IMPDH2 depletion. JunB inhibitor neutralized the IMPDH2-mediated increased phosphorylation of JunB. <P> Conclusion: Our findings, thus, suggest that IMPDH2 exhibits its oncogenic role in HB partially via JunB-dependent proliferation.</P>]]></description> </item><item><title><![CDATA[Anticancer Properties of Baicalin against Breast Cancer and other
Gynecological Cancers: Therapeutic Opportunities based on Underlying
Mechanisms]]></title><link>https://www.benthamscience.comarticle/138003</link><description><![CDATA[Gynecological cancers are serious life-threatening diseases responsible for high morbidity and mortality around the world. Chemotherapy, radiotherapy, and surgery are considered standard therapeutic modalities for these cancers. Since the mentioned treatments have undesirable side effects and are not effective enough, further attempts are required to explore potent complementary and/or alternative treatments. This study was designed to review and discuss the anticancer potentials of baicalin against gynecological cancers based on causal mechanisms and underlying pathways. Traditional medicine has been used for thousands of years in the therapy of diverse human diseases. The therapeutic effects of natural compounds like baicalin have been widely investigated in cancer therapy. Baicalin was effective against gynecological cancers by regulating key cellular mechanisms, including apoptosis, autophagy, and angiogenesis. Baicalin exerted its anticancer property by regulating most molecular signaling pathways, including PI3K/Akt/mTOR, NF&#954;B, MAPK/ERK, and Wnt/&#946;-catenin. However, more numerous experimental and clinical studies should be designed to find the efficacy of baicalin and the related mechanisms of action.]]></description> </item><item><title><![CDATA[Regulating miRNAs Expression by Resveratrol: Novel Insights based on
Molecular Mechanism and Strategies for Cancer Therapy]]></title><link>https://www.benthamscience.comarticle/135470</link><description><![CDATA[Resveratrol, a polyphenolic phytoalexin found in a wide range of plants, including grapes, berries, and peanuts, is an extensively researched phytochemical with unique pharmacological capabilities and amazing potential to affect many targets in various cancers. Resveratrol's anti-cancer activities are due to its targeting of a variety of cellular and molecular mechanisms and crucial processes involved in cancer pathogenesis, such as the promotion of growth arrest, stimulation of apoptosis, suppression of cell proliferation, induction of autophagy, regulating oxidative stress and inflammation, and improving the influence of some of the other chemotherapeutic agents. MicroRNAs (miRNAs) are non-coding RNAs that modulate gene expression by degrading mRNA or inhibiting translation. MiRNAs serve critical roles in a wide range of biological activities, and disruption of miRNA expression is strongly linked to cancer progression. Recent research has shown that resveratrol has anti-proliferative and/or pro-apoptotic properties via modulating the miRNA network, which leads to the inhibition of tumor cell proliferation, the activation of apoptosis, or the increase of traditional cancer therapy effectiveness. As a result, employing resveratrol to target miRNAs will be a unique and potential anticancer approach. Here, we discuss the main advances in the modulation of miRNA expression by resveratrol, as well as the several miRNAs that may be influenced by resveratrol in different types of cancer and the significance of this natural drug as a promising strategy in cancer treatment.]]></description> </item><item><title><![CDATA[Uncommon Metachronicity: Breast and Endometrial Carcinomas in a Young Woman with No Familial Cancer History - A Case Report]]></title><link>https://www.benthamscience.comarticle/138749</link><description><![CDATA[<p>Background: Worldwide, breast and endometrial carcinomas are the two most common cancers of women, but their coexistence in a woman <40 years of age is a rare event. The risk of developing a new second primary cancer is higher in cancer survivors compared to those without a history of cancer. The exact pathogenesis of two different primary malignancies is not clear. Still, the coexistence of breast and endometrial carcinoma may be due to germline mutations of p53, BRCA 1, and BRCA 2 genes, environmental, hereditary, and immune-mediated factors. </p> <p> Case Presentation: The present case report briefs the finding of a 37-year-old woman who presented to the Gynecological outpatient department with complaints of abnormal uterine bleeding and a solid irregular lump in the upper outer quadrant of the right breast and the right axilla. She had a history of modified radical mastectomy for left breast ductal carcinoma five years back. She was diagnosed as a case of metachronous endometrial carcinoma (stage IA) with a recurrence of invasive ductal carcinoma in the right breast with metastasis to the right axillary lymph node. </p> <p> Conclusion: The metachronous development of breast and endometrial carcinoma in young women is relatively rare. In young patients <40 years of age with gynecological or breast carcinoma, a thorough work-up, including genetic testing and follow-up, should be done for early diagnosis of metachronous or synchronous primary malignancies of other organs.</p>]]></description> </item><item><title><![CDATA[Anti-cancer Potential of Phytoflavonoidal Drugs against Gynecological Cancer]]></title><link>https://www.benthamscience.comarticle/138359</link><description><![CDATA[<p>Background: Flavonoids, one of the major bioactive constituents of herbal drugs, have been scientifically reported to possess diverse therapeutic potentials such as anticancer, immunomodulatory, neuroprotective, cardioprotective, antioxidant, etc. This manuscript enlightens the anticancer potential of traditional herbal flavonoids in gynecological cancer i.e., is one of the major life-threats in women. </p> <p> Objective: This manuscript is aimed at an insightful compilation of scientific substantiations of herbal flavonoids in gynecological cancer along with targeted drug delivery systems for the same. </p> <p> Materials and Methods: The contents and data represented in the article have been reviewed using institutional libraries and online database resources (available in the public domain) such as PubMed, Science-Direct, Web of Science, American Association of Pharmaceutical Scientists, Google Scholar, Hinari, SciFinder, Research Gate, etc. </p> <p> Results: Flavonoids are natural compounds and have potential against cervical, ovarian, and endometrial cancer. <i>In-vitro</i> and <i>in-vivo</i> experiments have demonstrated the significant potential of flavonoids in gynecological cancer, especially cervical, ovarian, and endometrial cancer. It was reported from in-vitro experimentations that targeted drug delivery system improves the anticancer effect of flavonoids. </p> <p> Conclusion: Phytoflavonoids have the potential to prevent gynecological cancer by induction of apoptosis cell cycle arrest and reactive oxygen species generation. Further studies on the drug delivery system of flavonoids are warranted.</p>]]></description> </item><item><title><![CDATA[Renal Lesions with Low-level Enhancement on Contrast-enhanced CT Promotes
Early Detection of Drug-induced Kidney Injury in Patients Administered Anticancer
Drugs]]></title><link>https://www.benthamscience.comarticle/139905</link><description><![CDATA[<p>Background: Some patients with cancer-administered anti-cancer drugs may develop renal lesions with low-level enhancement on follow-up abdominal computed tomography (CT). <p> Objective: To explore the clinical significance of renal lesions with low-level enhancement on CT after exposure to anti-cancer drugs. <p> Methods: Medical records of patients with cancer who developed renal lesions on CT after exposure to anti-cancer drugs were retrospectively reviewed. Renal lesions were scored according to the extent of involvement, CT attenuation values of lesions and normal parenchyma were measured on precontrast CT and three phases of contrast-enhanced CT, and changes in serum creatinine (SCr) from one week before exposure to drugs to one week before and after the appearance of renal lesions were recorded. <p> Results: This study included 54 patients (86 lesions). Lesions were slightly lower density on pre-contrast CT, and less enhancing than normal renal parenchyma, especially in the delayed phase. Lesions were wedge-shaped, and involved the renal pyramid and associated renal cortex, as well as, were single or multiple, and occurred in the unilateral or bilateral kidneys. There were patchy and cord-like shadows of increased density in adjacent perirenal adipose tissue. During follow-up, lesions disappeared in 15 patients and persisted in 39 patients without significant progression. There were significant differences in renal lesions and normal renal parenchyma CT attenuation values in each phase of contrast-enhanced CT. Change in SCr level was significantly positively correlated with lesion score. <p> Conclusion: Renal lesions with low-level enhancement on CT suggest early drug-induced kidney injury. These findings will inform clinical decision-making.</p>]]></description> </item><item><title><![CDATA[Using Apparent Diffusion Coefficient (ADC) of Endometrial Cancer MRI to
Determine P53 Molecular Subtypes]]></title><link>https://www.benthamscience.comarticle/139853</link><description><![CDATA[<p>Background: Endometrial Cancer (EC) is a highly heterogeneous cancer comprising both histological and molecular subtypes. Using a non-invasive modality method to trigger these subtypes as early as possible can aid clinicians in establishing individualized treatment. <p> Purpose: The study aimed to clarify the value of the Apparent Diffusion Coefficient (ADC) of EC MRI in determining molecular subtypes. <p> Material and Methods: We retrospectively recruited 109 patients with pathologically proven EC (78 endometrioid cancers and 31 non-endometrioid cancers) with available molecular classification from a tertiary centre. MRI was prospectively performed a month prior to surgery; images were blindly interpreted by two experienced radiologists with consensus reading. The ADC value was measured by an experienced radiologist on the commercially available processing workstation. Interoperator measurement consistency was calculated. <p> Results: Our sample comprised 17 PLOE, 32 MSI-H, 31 NSMP, and 29 P53abn ECs. Clinical information did not differ significantly among the groups. The maximum diameter and volume of the lesions differed among the groups. The ADC value in the maximal area (ADCarea) or region of interest (ROI, ADCroi) in the P53abn group was higher than that in the other groups (894.0 ±12.6 and 817.5 ± 83.3 x10-6 mm2/s). The ADC mean values were significantly different between the P53abn group and the other groups (P = 0.000). The nomogram showed the highest discriminative ability to distinguish P53abn EC from other types (AUC: 0.859). <p> Conclusion: Our results have suggested the quantitative MR characteristics (ADC values) derived from preoperative EC MRI to provide useful information in preoperatively determining P53abn cancer.</p>]]></description> </item><item><title><![CDATA[Endometrial Adenofibroma in a Patient Receiving Toremifene: A Case Report]]></title><link>https://www.benthamscience.comarticle/131218</link><description><![CDATA[<P>Introduction: Adenofibroma is a rare benign Müllerian mixed tumor composed of epithelial and mesenchymal cells. This tumor may occasionally be associated with toremifene therapy which is used as an adjuvant drug for breast cancer. <P> Case Presentation: We describe a case of a 55-year-old woman with adenofibroma of the endometrium. This patient was receiving toremifene after surgery and neoadjuvant chemotherapy for breast cancer. She underwent a total abdominal hysterectomy and bilateral salpingectomy. There was no evidence of tumor residual or recurrence at 32 months of MRI follow-up. <P> Conclusion: In conclusion, we report a rare case of endometrial adenofibroma in a patient receiving toremifene. It must be borne in mind that long-term toremifene therapy may increase the frequency of endometrial neoplasms.</P>]]></description> </item><item><title><![CDATA[Contrast-enhanced Ultrasound of Xanthogranulomatous Endometritis: A Case
Report and Literature Review]]></title><link>https://www.benthamscience.comarticle/131702</link><description><![CDATA[<P>Introduction: Xanthogranulomatous endometritis (XGE) is a rare inflammatory disease, which can easily misdiagnose as cancer in imaging diagnosis. Diagnosis of XGE relies on histopathological examination and immunohistochemistry. <P> Case Presentation: In this study, a case of a 72-year-old female with XGE and elevated CA125 is presented, which was misdiagnosed as endometrial cancer in transvaginal ultrasonography and ovarian cystadenocarcinoma in CT. However, the features of XGE on the contrast-enhanced ultrasound (CEUS) were different from that of endometrial cancer. The patient finally underwent laparoscopic hysterectomy and bilateral adnexectomy. <P> Discussion: The histopathological examination and immunohistochemistry suggested xanthogranulomatous endometritis (histiocytic endometritis). This case report manifests that CEUS may be a new noninvasive diagnostic method for XGE, which may reduce extensive tissue sampling and unnecessary hysterectomies for patients.</P>]]></description> </item><item><title><![CDATA[Image Quality Improvement of Low-dose Abdominal CT using Deep Learning
Image Reconstruction Compared with the Second Generation Iterative
Reconstruction]]></title><link>https://www.benthamscience.comarticle/132054</link><description><![CDATA[<p>Background: Whether deep learning-based CT reconstruction could improve lesion conspicuity on abdominal CT when the radiation dose is reduced is controversial. <p> Objectives: To determine whether DLIR can provide better image quality and reduce radiation dose in contrast-enhanced abdominal CT compared with the second generation of adaptive statistical iterative reconstruction (ASiR-V). <p> Aims: This study aims to determine whether deep-learning image reconstruction (DLIR) can improve image quality. <p> Methods: In this retrospective study, a total of 102 patients were included, who underwent abdominal CT using a DLIR-equipped 256-row scanner and routine CT of the same protocol on the same vendor&#039;s 64-row scanner within four months. The CT data from the 256-row scanner were reconstructed into ASiR-V with three blending levels (AV30, AV60, and AV100), and DLIR images with three strength levels (DLIR-L, DLIR-M, and DLIR-H). The routine CT data were reconstructed into AV30, AV60, and AV100. The contrast-to-noise ratio (CNR) of the liver, overall image quality, subjective noise, lesion conspicuity, and plasticity in the portal venous phase (PVP) of ASiR-V from both scanners and DLIR were compared. <p> Results: The mean effective radiation dose of PVP of the 256-row scanner was significantly lower than that of the routine CT (6.3±2.0 mSv vs. 2.4±0.6 mSv; p< 0.001). The mean CNR, image quality, subjective noise, and lesion conspicuity of ASiR-V images of the 256-row scanner were significantly lower than those of ASiR-V images at the same blending factor of routine CT, but significantly improved with DLIR algorithms. DLIR-H showed higher CNR, better image quality, and subjective noise than AV30 from routine CT, whereas plasticity was significantly better for AV30. <p> Conclusion: DLIR can be used for improving image quality and reducing radiation dose in abdominal CT, compared with ASIR-V.</p>]]></description> </item><item><title><![CDATA[Prediction of Lymphovascular Space Invision in Endometrial Cancer based on
Multi-parameter MRI Radiomics Model]]></title><link>https://www.benthamscience.comarticle/139262</link><description><![CDATA[<p>Objective: To explore the application value of a combined model based on multi-parameter MRI radiomics and clinical features in preoperative prediction of lymphatic vascular space invasion (LVSI) in endometrial carcinoma (EC). <p> Methods: This retrospective study collected the clinicopathological and imaging data of 218 patients with EC in Yuncheng Central Hospital from March 2018 to May 2022. The patients were randomly divided into training group (n=152) and validation group (n= 66) according to the ratio of 7: 3. Based on the ADC, CE-sag, CE-tra, DWI, T2WI-sag-fs, T2WI-tra sequence images of each patient, the region of interest was manually segmented and the features were extracted. The four-step dimensionality reduction method based on max-relevance and min-redundancy (MRMR) and least absolute shrinkage and selection operator (LASSO) regression was used for feature selection and radiomics model construction. Independent predictors of clinicopathological features were screened by multivariate logistic regression analysis. The imaging model based on ADC, CE-sag, CE-tra, DWI, T2WI-sag-fs, T2WI-tra single sequence and combined sequence and the fusion model with clinicopathological features were constructed, and the nomogram was made. ROC curve, correction curve and decision analysis curve were used to evaluate the efficacy and clinical benefits of the nomogram. <p> Results: There was no significant difference in general clinical data between the training and validation groups (P > 0.05). After screening the extracted features, 16 radiomics features were obtained, which were all related to LVSI in EC patients (P &#60; 0.05). The area under the ROC curve (AUC) of the six independent sequence radiomics models in the training group was 0.807, 0.794, 0.826, 0.794, 0.828, 0.824, respectively. The AUC corresponding to the radiomics model constructed by the combined sequence was 0.884, and the diagnostic efficiency was the best, which was verified in the validation group. The AUC of the nomogram constructed by the combined radiomics model and age maximum tumor diameter(MTD), lymph node enlargement (LNE) in the training group and the validation group were 0.914 and 0.912, respectively. The correction curve shows that the nomogram has good correction performance. The decision curve suggests that taking radiomics nomogram to predict LVSI net benefit when the risk threshold is > 10% is better than considering all patients as LVSI+ or LVSI-. <p> Conclusion: The combined model based on multi-parametric MRI radiomics features and clinical features has good predictive value for LVSI status in EC patients.</p>]]></description> </item><item><title><![CDATA[Differentiation of Borderline Epithelial Ovarian Tumors from Benign and
Malignant Epithelial Ovarian Tumors by MRI Scoring]]></title><link>https://www.benthamscience.comarticle/132325</link><description><![CDATA[<P>Introduction: The distinction between benign and borderline epithelial ovarian tumors is important because treatment and follow-up strategies differ. <P> Objective: We aimed to evaluate benign, borderline, and malignant epithelial ovarian tumors using MRI features and contributed to the preoperative evaluation. <P> Methods: MRIs of 81 patients (20 bilateral), including 31 benign, 27 borderline, and 23 malignant, who had pelvic imaging between 2013-2020, were evaluated retrospectively. The evaluation was made blindly to the pathology result by two radiologists with MRI scoring and features that we determined. MRI evaluation was performed with T1 TSE, T2 TSE, fat-suppressed T2 TSE, and before and after contrast T1 fat-suppressed and non-fat-suppressed TSE images. The numbers and findings obtained in scoring were evaluated by Chi-Square, ordinal logistic regression, and 2 and 3 category ROC analysis. <P> Results: The total score varied between 7 and 24. Among the three groups, a significant difference was found in terms of T1, T2 signal intensity (p <0.01), size (p = 0.055), solid area (p <0.001), septa number (p <0.05), ovarian parenchyma (p = 0.001), ascites (p <0.001), peritoneal involvement (p <0.001), laterality (p <0.001), contrast enhancement pattern (p <0.001). On the other hand, no significant difference was found in terms of wall thickness, lymph node involvement and endometrial thickness (p> 0.05). Cut-off values were found as 11.5 and 18.5 in the 3-category ROC analysis performed for the score (VUS: 0.8109). Patients with a score below 11.5 were classified as benign, those between 11.5-18.5 as borderline, and those over 18.5 as malignant. <P> Conclusion: The differentiation of borderline tumors from benign and malignant tumors by MRI scoring will contribute to the preoperative diagnosis.</P>]]></description> </item><item><title><![CDATA[Prolapsed Uterine Smooth Muscle Tumor of uncertain Malignant Potential: A
Case Report and Review of Radiological Findings]]></title><link>https://www.benthamscience.comarticle/132509</link><description><![CDATA[<p>Introduction: Uterine smooth muscle tumor of uncertain malignant potential (STUMP) is a rare tumor that arises in the myometrium of the uterus. It is regarded as an intermediate malignant tumor according to the recent World Health Organization classification. Few studies have reported the radiologic findings of STUMP, and the differentiation of STUMP from leiomyoma remains controversial. <p> Case Description: A 42-year-old nulliparous female presented at our institution with massive vaginal bleeding. Radiological studies, including ultrasonography, computed tomography (CT), and magnetic resonance imaging, revealed an oval-shaped mass with well-defined margins in the uterus protruding into the vagina. The patient underwent a total abdominal hysterectomy, and the final pathology was confirmed as STUMP. <p> Conclusion: Distinguishing STUMP from leiomyomas based solely on radiological findings can be challenging. However, if the uterine mass appears as a single mass lacking acoustic shadowing on ultrasound and demonstrates diffusion restriction with high T2 signal intensity on magnetic resonance imaging, consideration of STUMP may be necessary for proper patient management, given the poor prognosis associated with this tumor.</p>]]></description> </item><item><title><![CDATA[Value of Multimodal Diffusion-weighted Imaging in Preoperative Evaluation of
Ki-67 Expression in Endometrial Carcinoma]]></title><link>https://www.benthamscience.comarticle/133564</link><description><![CDATA[<p>Purpose: To investigate the value of multimodal diffusion weighted imaging (DWI) in preoperative evaluation of Ki-67 expression of endometrial carcinoma (EC). <p> Materials and Methods: Patients who had undergone pelvic DWI, intravoxel incoherent motion (IVIM), and diffusion kurtosis imaging (DKI) sequence MRI scan before surgery were retrospectively enrolled. Single index model, double index model, and DKI were used for post-processing of the DWI data, and the apparent diffusion coefficient (ADC), real diffusion coefficient (D), pseudo diffusion coefficient (D*), perfusion fraction (f), non-Gaussian mean diffusion kurtosis (MK), mean diffusion coefficient (MD) and anisotropy fraction (FA) were calculated and compared between the Ki-67 high (≥50%) and low (&#60;50%) expression groups. <p> Results: Forty-two patients with a median age of 56 (range 37 - 75) years were enrolled, including 15 patients with a high Ki-67 (≥50%) expression and 27 with a low Ki-67 (&#60;50%) expression. The MK (0.91 ± 0.12 vs. 0.76 ± 0.12) was significantly (P<0.05) higher while MD (0.99 ± 0.17 vs. 1.16 ± 0.22), D (0.55 ± 0.06 vs. 0.62 ± 0.08), and f (0.21 vs. 0.28) were significantly (P&#60;0.05) lower in the high than in the low expression group. The combined model of MK, MD, D, and f-values had the largest area under the curve (AUC) value of 0.869 (95% CI: 0.764-0.974), sensitivity 0.733 and specificity 0.852, followed by the MK value with an AUC value 0.827 (95% CI: 0.700-0.954), sensitivity 0.733 and specificity 0.815. <p> Conclusions: IVIM and DKI have certain diagnostic values for preoperative evaluation of the EC Ki-67 expression, and the combined model has the highest diagnostic efficiency.</p>]]></description> </item><item><title><![CDATA[MR Diffusion-Weighted Imaging in Evaluating Immediate HIFU Treatment
Response of Uterine Fibroids]]></title><link>https://www.benthamscience.comarticle/138807</link><description><![CDATA[<p>Background: Nowadays, High Intensity Focused Ultrasound (HIFU) is a common surgery option for the treatment of uterine fibroids in China, the immediate response of which is clinically evaluated using Contrast Enhanced (CE) imaging. However, the injection of gadolinium with its potential adverse effect is of concern in CE and therefore, it deserves efforts to find a better imaging method without the need for contrast agent injection for this task. <p> Objective: To assess the role of Diffusion-weighted Imaging (DWI) in evaluating the immediate therapeutic response of HIFU treatment for uterine fibroids in comparison with CE. <p> Methods: 68 patients with 74 uterine fibroids receiving HIFU treatment were enrolled, and immediate treatment response was assessed using post-surgical DWI images. Semi-quantitative ordinal ablation quality grading and quantitative nonperfusion volume (NPV) measurement based on DWI and CE imaging were determined by two experienced radiologists. Agreement of ablation quality grading between DWI and CE was assessed using the weighted kappa coefficient, while intraobserver, interobserver and interprotocol agreements of NPV measurements within and between DWI and CE were evaluated using the intraclass correlation (ICC) and Bland-Altman analysis. <p> Results: Grading of immediate HIFU treatment response showed a moderate agreement between DWI and CE (weighted kappa = 0.446, p &#60; 0.001). NPV measured in 65 fibroids with DWI of Grade 3~5 showed very high ICCs for the intraobserver and interobserver agreement within DWI and CE (all ICC > 0.980, p &#60; 0.001) and also for the interprotocol agreement between DWI and CE (ICC = 0.976, p &#60; 0.001). <p> Conclusion: DWI could provide satisfactory ablation quality grading, and reliable NPV quantification results to assess immediate therapeutic responses of HIFU treatment for uterine fibroids in most cases, which suggests that non-contrast enhanced DWI might be potentially used as a more costeffective and convenient method in a large proportion of patients for this task replacing CE imaging.</p>]]></description> </item><item><title><![CDATA[Assembling High-quality Lymph Node Clinical Target Volumes for Cervical
Cancer Radiotherapy using a Deep Learning-based Approach]]></title><link>https://www.benthamscience.comarticle/134611</link><description><![CDATA[<p>Aim: The study aimed to explore an approach for accurately assembling high-quality lymph node clinical target volumes (CTV) on CT images in cervical cancer radiotherapy with the encoder-decoder 3D network. <p> Methods: 216 cases of CT images treated at our center between 2017 and 2020 were included as a sample, which were divided into two cohorts, including 152 cases and 64 cases, respectively. Para-aortic lymph node, common iliac, external iliac, internal iliac, obturator, presacral, and groin nodal regions were delineated as sub-CTV manually in the cohort including 152 cases. Then, the 152 cases were randomly divided into training (96 cases), validation (36 cases), and test (20 cases) groups for the training process. Each structure was individually trained and optimized through a deep learning model. An additional 64 cases with 6 different clinical conditions were taken as examples to verify the feasibility of CTV generation based on our model. Dice similarity coefficient (DSC) and Hausdorff distance (HD) metrics were both used for quantitative evaluation. <p> Results: Comparing auto-segmentation results to ground truth, the mean DSC value/HD was 0.838/7.7mm, 0.853/4.7mm, 0.855/4.7mm, 0.844/4.7mm, 0.784/5.2mm, 0.826/4.8mm and 0.874/4.8mm for CTV_PAN, CTV_common iliac, CTV_internal iliac, CTV_external iliac, CTV_obturator, CTV_presacral, and CTV_groin, respectively. The similarity comparison results of six different clinical situations were 0.877/4.4mm, 0.879/4.6mm, 0.881/4.2mm, 0.882/4.3mm, 0.872/6.0mm, and 0.875/4.9mm for DSC value/HD, respectively. <p> Conclusion: We have developed a deep learning-based approach to segmenting lymph node sub-regions automatically and assembling high-quality CTVs according to clinical needs in cervical cancer radiotherapy. This work can increase the efficiency of the process of cervical cancer detection and treatment.</p>]]></description> </item><item><title><![CDATA[T1 Mapping and Amide Proton Transfer Weighted Imaging for Predicting
Lymph Node Metastasis in Patients with Rectal Cancer]]></title><link>https://www.benthamscience.comarticle/138395</link><description><![CDATA[<p>Background: Accurate preoperative judgment of lymph node (LN) metastasis is a critical step in creating a treatment strategy and evaluating prognosis in rectal cancer (RC) patients. <p> Objective: This study aimed to explore the value of T1 mapping and amide proton transfer weighted (APTw) imaging in predicting LN metastasis in patients with rectal cancer. <p> Methods: In a retrospective study, twenty-three patients with pathologically confirmed rectal adenocarcinoma who underwent MRI and surgery from August 2019 to August 2021 were selected. Then, 3.0T/MR sequences included conventional sequences (T1WI, T2WI, and DWI), APTw imaging, and T1 mapping. Patients were divided into LN metastasis (group A) and non-LN metastasis groups (group B). The intra-group correlation coefficient (ICC) was used to test the inter-observer consistency. Mann-Whitney U test was used to compare the differences between the two groups. Spearman correlation analysis was performed to evaluate the correlation between T1 and APT values. Logistic regression and receiver operating characteristic (ROC) curve analyses were performed to assess the differential performance of each parameter and their combination. The difference between AUCs was compared using the DeLong test. <p> Results: The APT value in patients with LN metastasis was significantly higher than in those without LN metastasis group (P=0.020). Also, similar results were observed for the T1 values (P=0.001). The area under the ROC curve of the APT value in the prediction of LN metastasis was 0.794; when the cutoff value was 1.73%, the sensitivity and specificity were 71.4% and 88.9%, respectively. The area under the ROC curve of the T1 value was 0.913; when the cutoff value was 1367.36 ms, the sensitivity and specificity were 78.6% and 100.0%, respectively. The area under the ROC curve of T1+APT was 0.929, with a sensitivity of 78.6% and specificity of 100.0%. <p> Conclusion: APT and T1 values show great diagnostic efficiency in predicting LN metastasis in rectal cancer.</p>]]></description> </item><item><title><![CDATA[SegEIR-Net: A Robust Histopathology Image Analysis Framework for Accurate
Breast Cancer Classification]]></title><link>https://www.benthamscience.comarticle/138388</link><description><![CDATA[<p>Background: Breast Cancer (BC) is a significant threat affecting women globally. An accurate and reliable disease classification method is required to get an early diagnosis. However, existing approaches lack accurate and robust classification. <p> Objective: This study aims to design a model to classify BC Histopathology images accurately by leveraging segmentation techniques. <p> Methods: This work proposes a combined segmentation and classification approach for classifying BC using histopathology images to address these issues. Chan-Vese algorithm is used for segmentation to accurately delineate regions of interest within the histopathology images, followed by the proposed SegEIR-Net (Segmentation using EfficientNet, InceptionNet, and ResNet) for classification. Bilateral Filtering is also employed for noise reduction. The proposed model uses three significant networks, ResNet, InceptionNet, and EfficientNet, concatenates the outputs from each block followed by Dense and Dropout layers. The model is trained on the breakHis dataset for four different magnifications and tested on BACH (BreAst Cancer Histology) and UCSB (University of California, Santa Barbara) datasets. <p> Results: SegEIR-Net performs better than the existing State-of-the-Art (SOTA) methods in terms of accuracy on all three datasets, proving the robustness of the proposed model. The accuracy achieved on breakHis dataset are 98.66%, 98.39%, 97.52%, 95.22% on different magnifications, and 93.33% and 96.55% on BACH and UCSB datasets. <p> Conclusion: These performance results indicate the robustness of the proposed SegEIR-Net framework in accurately classifying BC from histopathology images.</p>]]></description> </item><item><title><![CDATA[MRI Plain Scan: A Tool in the Management of Cervical Cancer during
Pregnancy]]></title><link>https://www.benthamscience.comarticle/138376</link><description><![CDATA[<p>Objective: The purpose of this study was to assess the diagnostic value of magnetic resonance imaging (MRI) in staging and treatment of cervical cancer in pregnancy, and to evaluate the benefit of apparent diffusion coefficient (ADC) during neoadjuvant chemotherapy management. <p> Materials and Methods: This was a retrospective cohort study. Patients were divided into two groups according to the stage of cervical cancer. The mean term of pregnancy at the time of the diagnosis was the early second trimester (range 10-27 weeks) and the median age was 33 years (range 26-40 years). The abdominal and pelvic MRI images and clinical data of these patients were reviewed. Tumor size, local tumor spread, and nodal involvement were evaluated using an MRI dataset. The treatment and follow-up imaging were analyzed as well, and the ADC was measured before and after the chemotherapy. <p> Results: 16 patients with histopathologically confirmed cervical cancer during pregnancy were retrospectively enrolled. 7 patients were diagnosed with local cervical cancer (FIGO stage IAI) and designated as early stage group, as the lesion was invisible on MRI. In this group, pregnancies were allowed to continue until cesarean delivery (CD) at 38-41 weeks. The other 9 patients presenting with local or extensive cervical cancer (FIGO stage IB2-IIA2) were designated as the advanced-stage group. The lesion could be measured and analyzed on MRI. They were treated with neoadjuvant chemotherapy in pregnancy. Among them, 6 patients underwent TP regimen (paclitaxel 135~175 mg/m2 plus cisplatin 70~75 mg/m2), while 3 patients received TC regimen (paclitaxel 135~175 mg/m2 plus carboplatin AUC=5). NACT was performed for 1 to 2 courses before surgery. ADC demonstrated significant differences before and after chemotherapy administered during pregnancy (1.06 ± 0.12 sec/mm2 vs. 1.34 ± 0.21 sec/mm2). <p> Conclusion: MRI has been found to be helpful in staging cervical cancer in pregnancy. Patients with stage IA confirmed by MRI can choose conservative treatment and continue the pregnancy until term birth. MRI can dynamically monitor the efficacy of chemotherapy for patients with stage IB and above during pregnancy. ADC value can have a potential role in the evaluation of chemotherapy efficacy.</p>]]></description> </item><item><title><![CDATA[A Multimodal Ultrasound Observation Study on the Effect of Vitamin D on
Uterine Fibroids in Non-menopausal Women]]></title><link>https://www.benthamscience.comarticle/135748</link><description><![CDATA[<p>Introduction: It has been reported in the literature that Vitamin D can inhibit the growth of uterine fibroids, but the evaluation index is only the size of the uterine fibroids. The purpose of this study was to evaluate the effect of vitamin D on the size, hardness, and blood flow of uterine fibroids in premenopausal women by multimodal ultrasound. <p> Methods: A total of 64 pre-menopausal women with uterine fibroids complicated vitamin D deficiency were enrolled in this study and randomly divided into two groups: the vitamin D group (n=32) which received oral vitamin D (1600 IU/ day) and the control group (n=32) without vitamin D supplementation. After three months of intervention, the mean diameter of uterine fibroids, elastic strain ratio, and blood flow grade were evaluated by multimodal ultrasound, and the clinical symptoms of the two groups were evaluated by questionnaire. <p> Results: The vitamin D group reported a significant increment in the serum 25-hydroxyvitamin D (P &#60; 0.001). In addition, there were significant reductions in the mean diameter, and elastic strain ratio of uterine fibroids (P =.043 and P =.038, respectively), but no significant difference in the blood flow grade of uterine fibroids was observed (P =.272). Compared with the control group, the vitamin D group achieved significant relief in dysmenorrhea and frequent urination, as well as improvement in heavy menstrual bleeding. <p> Conclusion: The application of multimodal ultrasound provides a more comprehensive theoretical basis for vitamin on uterine fibroids. Vitamin D can effectively reduce the size of uterine fibroids in pre-menopausal women and relieve their symptoms. It is highly likely to be a promising, safe, effective, and inexpensive drug for uterine fibroids, which has good application value and promotion prospects.</p>]]></description> </item><item><title><![CDATA[The Significance of Contrast-enhanced Ultrasound in the Application of
Lymphaticovenous Anastomosis]]></title><link>https://www.benthamscience.comarticle/136386</link><description><![CDATA[<p>Background: Lymphaticovenous anastomosis (LVA) surgery is an effective treatment for lymphedema. Accurate evaluation and localization of the superficial lymphatic vessels before the operation is crucial for the success of the operation. Contrast-enhanced ultrasound (CEUS) is a new ultrasound technology, and its clinical application value in LVA surgery has not been established. <p> Objective: This study aimed to assess the efficacy of CEUS in LVA surgery and provide a novel approach for the clinical assessment and localization of superficial lymphatic vessels. <p> Methods: Retrospective analysis of imaging and surgical data was performed on 20 LVA patients. Among them, 10 cases underwent evaluation and localization using indocyanine green (ICG) lymphatic imaging (Group A), while 10 cases were evaluated and localized using CEUS (Group B). The differences in surgical data between the two groups were compared and analyzed. <p> Results: All 20 patients were female (mean age, 57.7 years ± 6.3 [SD]). CEUS demonstrated superior visualization and localization of superficial lymphatic vessels. The average diameter of lymphatic vessels identified in the CEUS group was significantly greater than that in the ICG group (0.78±0.06 vs. 0.52±0.05mm; P&#60;0.001). The duration of operation in group B was significantly shorter than that in group A (4.47±0.37 vs. 6.70±0.45mm; P&#60;0.001). The number of anastomosed lymphatic vessels in group B was less than that in group A [5.0(4.0, 6.0) vs. 9.5 (9.0, 11.3); P&#60;0.001]. <p> Conclusion: CEUS can serve as a viable alternative to ICG lymphatic imaging, facilitating improved lymphatic venous anastomosis surgery.</p>]]></description> </item><item><title><![CDATA[Insights into the Biological Properties of Prostate Cancer Stem Cells: Implications for Cancer Progression and Therapy]]></title><link>https://www.benthamscience.comarticle/137701</link><description><![CDATA[Prostate cancer (PCa) is the second prevalent cancer in men. Recent studies have highlighted the critical role of prostate cancer stem cells (PCSCs) in driving tumor initiation and metastasis of the prostate tissue. PCSCs are a rare population of cells in the prostate that possess self-renewal and differentiation capabilities, making them a potential therapeutic target for effective PCa treatment. Therefore, targeting PCSCs might be a novel strategy for the treatment of PCs. Research has shown that various signaling pathways, such as Notch, SHH, TGF-β, Wnt, STAT3, AKT, and EGFR, are involved in regulating PCSC proliferation, migration, and invasion. Additionally, non-coding RNAs, such as long ncRNAs and miRNAs, have emerged as critical regulators of PCSC pathogenesis and drug resistance. Here, we highlight that targeting these pathways could offer new opportunities for the management of PCa. This review summarizes the current knowledge surrounding the essential signaling pathways implicated in PCSC tumorigenesis and invasiveness.]]></description> </item><item><title><![CDATA[Impact of COVID-19 on Endometriosis Patients: An Integrative Review]]></title><link>https://www.benthamscience.comarticle/137864</link><description><![CDATA[<p>Background: During the COVID-19 pandemic, people's lives worldwide have undergone extensive changes. The pandemic has worsened the condition of patients with chronic diseases like women with endometriosis. </p> <p> Objective: This study aims to summarize available evidence on the impact of the COVID-19 pandemic on physical symptoms, mental health, and medical care of patients with endometriosis. </p> <p> Methods: In the present integrative review using PRISMA guidelines, related articles published from December 2019 to July 2023 in databases including MEDLINE, Science Direct, Scopus, and Google Scholar in the English language were extracted. </p> <p> Results: After evaluating the criteria for inclusion and exclusion, a total of 23 articles were chosen and examined. This study represents an open window to investigate the impact of COVID-19 on women with endometriosis. The COVID-19 pandemic has affected the symptoms, mental well-being, and medical care of women with endometriosis. </p> <p> Conclusions: There is a perceived necessity to provide supportive care for patients during pandemic restrictions. Remote work has had an unanticipated advantage, and it is recommended that women with endometriosis continue to work from home after COVID-19 to maintain their workplace effectiveness.</p>]]></description> </item><item><title><![CDATA[A Complete Overview of the Polycystic Ovarian Syndrome with Recent Advancement in Clinical Trial]]></title><link>https://www.benthamscience.comarticle/137430</link><description><![CDATA[<p>Background: Polycystic ovarian syndrome (PCOS) has emerged as one of the most common endocrine and metabolic disorders seen in women of childbearing age throughout the whole world. The complex pathophysiology, different diagnostic criteria, and various manifestations attached to several environmental factors, including lifestyle influences, have made it one of the most difficult disorders to treat in recent times. In addition, inadequate knowledge among patients and a lack of dedicated approved medications have only enhanced the difficulties in treating such a heterogeneous disorder. </p> <p> Objective: The main objective of this review-type paper is to provide a detailed overview of PCOS along with the current concept of a clinical stance in this complex multigenic disorder. </p> <p> Method : The following databases were used for literature searches: PubMed, Frontiers, Science Direct, Springer, Wiley, and MDPI. For the purpose of finding pertinent articles and contents, the keywords “PCOS; hirsutism; psychological burden; obesity” and others of a similar nature were utilized. </p> <p> Conclusion: PCOS is a complicated hormonal, metabolic, and psychological condition with many different clinical manifestations. It is among the most prevalent causes of infertility. Before considering any medication choices, lifestyle modifications should be considered the primary therapeutic prescription for PCOS-related infertility. According to recent studies, PCOS does not affect the risk of ovarian or breast cancer, but it does raise the risk of endometrial cancer in women of all ages. These results suggest that PCOS may increase the risk of gynaecological cancer morbidity. The following stage is ovulation stimulation, which is best accomplished with letrozole and is followed by clomiphene citrate. Women who had not responded to the first-line oral ovulatory medicine were given gonadotropins as a backup. Early detection of girls with a high propensity to develop PCOS will be made possible by a comprehensive knowledge of the condition's etiology. Adolescent PCOS will be better managed overall, related comorbidities will be prevented, and quality of life will increase with customized therapeutic approaches.</p>]]></description> </item><item><title><![CDATA[Treatment of Menopausal Symptoms with Herbal Medicines: A Review]]></title><link>https://www.benthamscience.comarticle/136348</link><description><![CDATA[<p>Background: Menopause refers to the natural process of the “cessation of the menstrual cycle.” This phase predominantly affects aged women and can lead to various symptoms such as hot flashes, insomnia, night sweats, and sexual dysfunction, among others. Unfortunately, many women remain unaware of this condition, and some even choose to overlook the symptoms. However, those who recognize the symptoms consult with a doctor, who may recommend Hormone replacement therapy (HRT). Initially, Hormone replacement therapy (HRT) can be effective, but prolonged use can result in side effects. To mitigate these effects, there is a need to explore and investigate herbal therapies as an alternative treatment for menopausal symptoms. </p> <p> Objective: The objective of this review is to explore and summarize various herbs used in managing menopausal symptoms as an alternative to hormone replacement therapy. Methods: For this review, we conducted a literature survey spanning from 1998 to 2023. We used keywords such as menopause, endocrinology, hormone replacement therapy, and herbs used for reducing menopausal symptoms to search databases such as Google Scholar, PubMed, and SciDirect. Relevant data were sourced from various journals like Plos One, JAMA, Frontier, Drug in Context, MDPI, Molecules, BMC Women's Health, Research Gate, Heliyon, Elsevier, Taylor & Francis, Nutrients, JMM, Wiley, OXFORD, Hindawi, Clinical Phytoscience, Pharmaceuticals, Phytomedicine, and Menopause: The Journal of The North American Menopause Society. </p> <p> Results: The literature review encompassed 40 research articles and 200 review articles, including randomized controlled trials. The findings revealed that several herbal plants, including <i>Curcuma longa, Zingiber officinale, Foeniculum vulgare, Trigonella foenum, Actaea racemosa, Glycyrrhiza glabra, Oenothera biennis, Trifolium pratense, Humulus lupulus, Vitex agnus-castus, Valeriana officinalis, Linum usitatissimum, Cannabis sativa</i>, and <i>Asparagus racemosus</i>, have shown efficacy in treating menopausal symptoms. </p> <p> Conclusion: In conclusion, medicinal plants can play a significant role in managing acute menopausal syndrome. The intent of this review is to highlight the most recent research on estrogenic plants for medicinal purposes and their therapeutic impact on cognitive deficiencies brought on by estrogen shortage during menopause and aging.</p>]]></description> </item><item><title><![CDATA[Network Subgraph-based Method: Alignment-free Technique for Molecular Network Analysis]]></title><link>https://www.benthamscience.comarticle/138608</link><description><![CDATA[<p> Background: Comparing directed networks using the alignment-free technique offers the advantage of detecting topologically similar regions that are independent of the network size or node identity. </p> <p> Objective: We propose a novel method to compare directed networks by decomposing the network into small modules, the so-called network subgraph approach, which is distinct from the network motif approach because it does not depend on null model assumptions. </p> <p> Method: We developed an alignment-free algorithm called the Subgraph Identification Algorithm (<i>SIA</i>, which could generate all subgraphs that have five connected nodes (5-node subgraph). There were 9,364 such modules. Then, we applied the <i>SIA</i> method to examine 17 cancer networks and measured the similarity between the two networks by gauging the similarity level using Jensen- Shannon entropy (<i>HJS</i>). </p> <p> Results: We identified and examined the biological meaning of 5-node regulatory modules and pairs of cancer networks with the smallest <i>HJS</i> values. The two pairs of networks that show similar patterns are (i) endometrial cancer and hepatocellular carcinoma and (ii) breast cancer and pathways in cancer. Some studies have provided experimental data supporting the 5-node regulatory modules. </p> <p> Conclusion: Our method is an alignment-free approach that measures the topological similarity of 5-node regulatory modules and aligns two directed networks based on their topology. These modules capture complex interactions among multiple genes that cannot be detected using existing methods that only consider single-gene relations. We analyzed the biological relevance of the regulatory modules and used the subgraph method to identify the modules that shared the same topology across 2 cancer networks out of 17 cancer networks. We validated our findings using evidence from the literature.</p>]]></description> </item><item><title><![CDATA[The Prognostic Value and Clinical Significance of lncRNA SNHG5 Expression in Patients with Multiple Malignancies: A Bioinformatic and Meta-analysis]]></title><link>https://www.benthamscience.comarticle/138740</link><description><![CDATA[<p>Background: Long non-coding RNA small nucleolar RNA host gene 5 (lncRNA SNHG5) has been identified as both a promising target for treatment and a predictor of prognosis in diverse types of cancer. The objective of this study was to assess whether lncRNA SNHG5 expression can be utilized as a prognostic biomarker for human cancer. </p> <p> Methods: To ensure a thorough search of the literature for relevant English studies published before July 2023, several databases were searched, including PubMed, Web of Science, ProQuest, Cochrane Library, and Google Scholar. The study evaluated the impact of lncRNA SNHG5 on the overall survival (OS) of cancer by calculating the pooled hazard ratio (HR) and odds ratio (OR) with 95% confidence intervals (CIs). To further confirm the accuracy of the findings, the study investigated the expression profile and prognostic significance of lncRNA SNHG5 through the use of GenomicScape, OncoLnc, Kaplan-Meier plotter, and GEPIA databases. </p> <p> Results: In this study, 995 patients were examined across a total of fourteen original studies. The findings indicated that there was a significant relationship between heightened lncRNA SNHG5 expression and reduced OS, as evidenced by both univariate and multivariate analyses (HR = 1.89; 95% CI, 1.44-2.49; p &#60; 0.001; HR = 3.97; 95% CI, 1.80-8.73; p &#60; 0.001, respectively). Pooled OR analysis showed a significant association between over-expression of lncRNA SNHG5 with advanced histological grade (OR = 0.28; 95% CI, 0.11-0.71; p = 0.007), present lymph node metastasis (LNM; OR = 4.28; 95% CI, 2.47-7.43; p &#60; 0.001), and smoking history (OR = 0.27; 95% CI, 0.15-0.49; p &#60; 0.001). Bioinformatic databases confirmed that elevated SNHG5 expression was significantly linked to poor prognosis in cancer patients, including colorectal cancer (CRC), acute myeloid leukemia (AML), and esophageal adenocarcinoma (ESAD), and a longer OS in patients with uterine corpus endometrial carcinoma (UCEC). </p> <p> Conclusion: These results suggest that lncRNA SNHG5 may serve as an adverse prognostic biomarker in several human cancers. Further investigations are needed to better understand the underlying mechanisms that link lncRNA SNHG5 to multiple malignancies.</p>]]></description> </item><item><title><![CDATA[Role of Vitamin D in Gynecological Cancer: State of the Art]]></title><link>https://www.benthamscience.comarticle/137685</link><description><![CDATA[Vitamin D and Vitamin D Receptors have gained more importance beyond their roles in bone metabolism and calcium homeostasis. Several epidemiological studies have confirmed that vitamin D has a specific function in a wide variety of gynecological cancers, such as ovarian cancer, endometrial cancer, cervical cancer, uterine fibroid, and vulvar cancer. The different anti-cancer mechanisms exerted by vitamin D on tumor cells are cell proliferation, cancer progression, angiogenesis, cell cycle arrest, and inflammation. The role of vitamin D is well emphasized in ovarian cancer and uterine fibroids, with limited studies available on cervical cancer and other types of gynecological cancers. Overall, most epidemiological data support that inadequate or low levels of vitamin D in the circulation are associated with risk and poor prognosis in several types of gynecological cancer. It is evident that vitamin D plays a prominent role as an anticancer agent against numerous types of cancer. This review focuses on the etiology and role of vitamin D and the Vitamin D Receptor in various types of gynecological cancer, as well as the mechanism of Vitamin D and its metabolites in the management of gynecological cancer.]]></description> </item><item><title><![CDATA[Mesenchymal Stem Cell Transplantation in Type 1 Diabetes Treatment:
Current Advances and Future Opportunity]]></title><link>https://www.benthamscience.comarticle/135081</link><description><![CDATA[Type 1 Diabetes (T1D) is characterized by hyperglycemia, and caused by a lack of insulin secretion. At present there is no cure for T1D and patients are dependent on exogenous insulin for lifelong, which seriously affects their lives. Mesenchymal stem cells (MSCs) can be differentiated to β cell-like cells to rescue the secretion of insulin and reconstruct immunotolerance to preserve the function of islet β cells. Due to the higher proportion of children and adolescents in T1D patients, the efficacy and safety issue of the application of MSC’s transplant in T1D was primarily demonstrated and identified by human clinical trials in this review. Then we clarified the mechanism of MSCs to relieve the symptom of T1D and found out that UC-MSCs have no obvious advantage over the other types of MSCs, the autologous MSCs from BM or menstrual blood with less expanded ex vivo could be the better choice for clinical application to treat with T1D through documentary analysis. Finally, we summarized the advances of MSCs with different interventions such as genetic engineering in the treatment of T1D, and demonstrated the advantages and shortage of MSCs intervened by different treatments in the transplantation, which may enhance the clinical efficacy and overcome the shortcomings in the application of MSCs to T1D in future.]]></description> </item><item><title><![CDATA[The Effect of Coronavirus Pandemic on the Treatment of Gynecological
and Breast Cancers]]></title><link>https://www.benthamscience.comarticle/134050</link><description><![CDATA[<p>Introduction: During the COVID-19 pandemic, various groups, including women with cancer, were affected as a high-risk group in terms of disease diagnosis and treatment. Despite the importance of therapeutic changes in cancers, such as breast and gynecological cancer, there is no comprehensive study in this regard that also refers to the coronavirus. The need for a deep understanding of the impact of coronavirus on the treatment plan of this group of patients caused the researcher to design and implement this study that aims to investigate the treatment challenge among cancer patients during the COVID-19 pandemic. </p> <p> Materials and Methods: To answer the study question, a comprehensive search was carried out in databases, such as PubMed, Web of Science Core Collection, and Scopus, using keywords, including cancer, gynecologic cancer, breast cancer, treatment, delay, and modification. Full-texted, English language and original articles were included in this study. </p> <p> Results: In total, 27 articles were selected for the study. The findings of this study revealed that COVID-19 greatly affects the treatment of gynecology and breast cancer. These patients experience delay or modification of cancer treatment. Increased time between diagnosis and treatment, delay, change or cancellation of surgery and change in treatment plan are the most important changes in cancer treatment during the COVID-19 pandemic. </p> <p> Conclusion: The COVID-19 pandemic has had a significant impact on various aspects of gynecology and breast cancer care worldwide. In the current pandemic, there has been a significant delay in the diagnosis and treatment of gynecological and breast cancer, which, due to its higher morbidity and mortality, has made the condition more difficult for cancer patients and treatment teams.</p>]]></description> </item><item><title><![CDATA[Contribution of Pelvic Ultrasonography in Perimenopausal Abnormal
Uterine Bleeding]]></title><link>https://www.benthamscience.comarticle/134878</link><description><![CDATA[<p>Background: About 70% of gynecological consultations for women in perimenopause are due to metrorrhagia. In most cases, they are only the witness of hormonal disturbances resulting from a luteal deficiency. Transvaginal ultrasound is the first innocuous and available additional examination that is requested as part of an etiological assessment. </p> <p> Objective: Our study aims to evaluate the contribution of ultrasonography in perimenopausal metrorrhagia and investigate possible clinical-ultrasound correlation. </p> <p> Methods: This analytical descriptive study was carried out on 50 treated for perimenopausal metrorrhagia in the emergency department of the Tunis Maternity and Neonatology Center for four months (November 1, 2017, to February 28, 2018). We included in our study patients who were not yet postmenopausal who were ≥ 45 years of age, and who sought care for breakthrough bleeding. All patients in our study initially underwent endovaginal ultrasonography, sometimes coupled with suprapubic ultrasonography. </p> <p> Results: The mean age of our patients was 46.3 years. Pelvic ultrasonography revealed an enlarged uterus in 16 patients (32%), with 14 of them having fibromatous uteri measuring between 3 to 10 centimeters. The findings indicate no significant correlation between ultrasound results and bleeding abundance (P = 0.321), pelvic pain (P = 0.108), and general condition (P = 0.437). </p> <p> Conclusion: Endovaginal pelvic ultrasonography is a quick, painless test and is the first test to be done first in an emergency department with perimenopausal vaginal bleeding. The correlation between clinical and ultrasound findings is highly random, making it impossible to assume a well-- coded diagnostic and therapeutic presumption.</p>]]></description> </item><item><title><![CDATA[Essential Fatty Acids along the Women’s Life Cycle and Promotion of a
Well-balanced Metabolism]]></title><link>https://www.benthamscience.comarticle/135152</link><description><![CDATA[Linoleic acid (&#969;-6 LA) and &#945;-linolenic acid (&#969;-3 ALA) are essential fatty acids (EFA) for human beings. They must be consumed through diet and then extensively metabolized, a process that plays a fundamental role in health and eventually in disease prevention. Given the numerous changes depending on age and sex, EFA metabolic adaptations require further investigations along the women’s life cycle, from onset to decline of the reproductive age. Thus, this review explains women’s life cycle stages and their involvement in diet intake, digestion and absorption, the role of microbiota, metabolism, bioavailability, and EFA fate and major metabolites. This knowledge is crucial to promoting lipid homeostasis according to female physiology through well- directed health strategies. Concerning this, the promotion of breastfeeding, nutrition, and physical activity is cardinal to counteract ALA deficiency, LA/ALA imbalance, and the release of unhealthy derivatives. These perturbations arise after menopause that compromise both lipogenic and lipolytic pathways. The close interplay of diet, age, female organism, and microbiota also plays a central role in regulating lipid metabolism. Consequently, future studies are encouraged to propose efficient interventions for each stage of women's cycle. In this sense, plant-derived foods and products are promising to be included in women’s nutrition to improve EFA metabolism.]]></description> </item><item><title><![CDATA[A Complex Condition; Polycystic Ovary Syndrome (PCOS): A Review of
its Recent Advanced Treatment]]></title><link>https://www.benthamscience.comarticle/136054</link><description><![CDATA[Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder affecting women worldwide. It refers to a condition that often has ‘poly’ liquid containing sacks around ovaries. It affects reproductive-aged females, giving rise to menstrual and related reproductive issues. PCOS is marked by hormonal imbalance, often resulting in hyperandrogenism. Women with PCOS might experience abnormal insulin activity and complications such as acne, mood swings, hirsutism, obesity, and infertility. The disease is linked with severe clinical ailments such as type 2 diabetes (T2DM), cardiovascular diseases (CVDs), and cancer. A faulty lifestyle, neuroendocrine factors, genetic causes, and androgen exposures often cause PCOS. The approach of society towards physiological problems such as PCOS in women is that it must be under the veil that is the ultimate barrier to the early diagnosis of PCOS. Thus, this review summarizes the causes, symptoms, pathophysiology, diagnosis, and possible treatment (medical, herbal, and lifestyle improvement, acupuncture, and bariatric surgery) related to PCOS.]]></description> </item><item><title><![CDATA[Curcumin Inhibits Vasculogenic Mimicry <i>via</i> Regulating ETS-1 in Renal
Cell Carcinoma]]></title><link>https://www.benthamscience.comarticle/138191</link><description><![CDATA[<p>Background: Metastatic renal cell carcinoma (RCC) poses a huge challenge once it has become resistant to targeted therapy. Vasculogenic mimicry (VM) is a novel blood supply system formed by tumor cells that can circumvent molecular targeted therapies. As one of the herbal remedies, curcumin has been demonstrated to play antineoplastic effects in many different types of human cancers; however, its function and mechanism of targeting VM in RCC remains unknown. <p> </p> Objective: Here, in the work, we explored the role of curcumin and its molecular mechanism in the regulation of VM formation in RCC. <p> </p> Methods: RNA-sequencing analysis, immunoblotting, and immunohistochemistry were used to detect E Twenty Six-1(ETS-1), vascular endothelial Cadherin (VE-Cadherin), and matrix metallopeptidase 9 (MMP9) expressions in RCC cells and tissues. RNA sequencing was used to screen the differential expressed genes. Plasmid transfections were used to transiently knock down or overexpress ETS-1. VM formation was determined by tube formation assay and animal experiments. CD31-PAS double staining was used to label the VM channels in patients and xenograft samples. <p> </p> Results: Our results demonstrated that VM was positively correlated with RCC grades and stages using clinical patient samples. Curcumin inhibited VM formation in dose and time-dependent manner <i>in vitro</i>. Using RNA-sequencing analysis, we discovered ETS-1 as a potential transcriptional factor regulating VM formation. Knocking down or overexpression of ETS-1 decreased or increased the VM formation, respectively and regulated the expression of VE-Cadherin and MMP9. Curcumin could inhibit VM formation by suppressing ETS-1, VE-Cadherin, and MMP9 expression both <i>in vitro</i> and <i>in vivo</i>. <p> </p> Conclusion: Our finding might indicate that curcumin could inhibit VM by regulating ETS-1, VE-Cadherin, and MMP9 expression in RCC cell lines. Curcumin could be considered as a potential anti-cancer compound by inhibiting VM in RCC progression.</p>]]></description> </item><item><title><![CDATA[The Role of Bile Acids in Pancreatic Cancer]]></title><link>https://www.benthamscience.comarticle/137979</link><description><![CDATA[Bile acids are well known to promote the digestion and absorption of fat, and at the same time, they play an important role in lipid and glucose metabolism. More studies have found that bile acids such as ursodeoxycholic acid also have anti-inflammatory and immune-regulating effects. Bile acids have been extensively studied in biliary and intestinal tumors but less in pancreatic cancer. Patients with pancreatic cancer, especially pancreatic head cancer, are often accompanied by biliary obstruction and elevated bile acids caused by tumors. Elevated total bile acid levels in pancreatic cancer patients usually have a poor prognosis. There has been controversy over whether elevated bile acids are harmful or beneficial to pancreatic cancer. Still, there is no doubt that bile acids are important for the occurrence and development of pancreatic cancer. This article summarizes the research on bile acid as a biomarker and regulation of the occurrence, development and chemoresistance of pancreatic cancer, hoping to provide some inspiration for future research.]]></description> </item><item><title><![CDATA[Uterine Cancer: A Nine-year Review from a Tertiary Hospital in Tamil
Nadu]]></title><link>https://www.benthamscience.comarticle/133283</link><description><![CDATA[<P>Background: With increasing uterine cancer in developing nations, there is a need for timely determination of the diagnosis, prognosis, and management options to reduce morbidity and mortality. <P> Objective: To analyze the socio-demographic, etio-pathological features and management of uterine cancer and evaluate its correlation with grading/staging in our population. <P> Methods: This retrospective descriptive study analyzed data from 97 histologically proven uterine cancer cases. Age, parity, symptoms, co-morbidities, body mass index (BMI), ultrasound features, histopathology type, stage and grade of the tumor, type of hysterectomy done, complications and mortality were analysed. Statistical analysis was done using ANOVA and chi-square test, and a p-value<0.05 indicated statistical significance. <P> Results: The mean age of diagnosis was 57.91 years, and the mean BMI was 29.32 Kg/m<sup>2</sup>. Majority of the patients were multiparous (42.27%), and only 10% were nulliparous. The disease was detected at an earlier age in nulliparous and obese women. Diabetes and hypertension were found in 75.25%. Most of the patients were detected with stage I cancer (80.6%). Patients diagnosed with uterine cancer on biopsy were treated with total abdominal hysterectomy with bilateral salpingo-oophorectomy andbilateral pelvic lymph node dissection (55.8%). Over 36% of patients received postop radiotherapy and/or chemotherapy. 21% patients were lost to follow-up and 12.37% died. Also, 24 cases had postoperative complications (wound infection). <P> Conclusion: Uterine cancer is common among obese women with diabetes and hypertension. In nulliparous and the obese, the cancer was detected at an earlier age. Most of our patients had stage 1 disease, and 90% was endometroid cancer. The study highlights the importance of endometrial sampling before hysterectomy in perimenopausal women to avoid suboptimal surgery in patients diagnosed with uterine cancer after a simple hysterectomy.</P>]]></description> </item><item><title><![CDATA[A Comparison of Self-esteem, Body Image, and Depression in
Hysterectomized and Non-hysterectomized Iranian Women: A Comparative
Cross-sectional Study]]></title><link>https://www.benthamscience.comarticle/133690</link><description><![CDATA[<P>Background: Hysterectomy is one of the factors that may affect women's body image and self-esteem and lead to serious psychological complications. <P> Objective: The study aimed to compare self-esteem, body image, and depression in hysterectomized and non-hysterectomized Iranian women. <P> Methods: In this cross-sectional comparative study, 140 women of the reproductive age, who have undergone hysterectomy with benign causes, were compared in terms of self-esteem, body image, and depression with 140 women receiving medical treatment due to abnormal bleeding in educational and medical centers in Tabriz, Iran. Sampling was conducted by convenience method. Self-esteem was assessed with the Rosenberg self-esteem questionnaire, body image was assessed with the multidimensional body-self relations questionnaire, and depression was assessed with the Beck II depression inventory. Data were analyzed by Pearson correlation test, independent t-test, chi-square test, and general linear model. <P> Results: The mean (standard deviation) of the body image in hysterectomized and nonhysterectomized women was 235.3 (28.5) and 250.1 (23.4) out of an achievable score of 69-395, respectively. The mean (standard deviation) self-esteem score for hysterectomized women was 20.4 (4.8) and it was 24.2 (3.4) in non-hysterectomized women (out of an achievable score of 0-30). The mean (standard deviation) depression score was 18.1 (9.7) and 5.5 (4.6) out of 0-63 in hysterectomized and non-hysterectomized women, respectively. The differences in self-esteem, body image, and depression variables were statistically significant in hysterectomized and non-hysterectomized women, respectively (P<0.001). <P> Conclusion: According to the results of the present study, the body image and self-esteem in hysterectomized women were low compared to non-hysterectomized women, while the level of depression was high, and this difference was statistically significant.</P>]]></description> </item><item><title><![CDATA[Multiomics Analysis of Disulfidptosis Patterns and Integrated
Machine Learning to Predict Immunotherapy Response in Lung
Adenocarcinoma]]></title><link>https://www.benthamscience.comarticle/140043</link><description><![CDATA[<p>Background: Recent studies have unveiled disulfidptosis as a phenomenon intimately associated with cellular damage, heralding new avenues for exploring tumor cell dynamics. We aimed to explore the impact of disulfide cell death on the tumor immune microenvironment and immunotherapy in lung adenocarcinoma (LUAD). <p> Methods: We initially utilized pan-cancer transcriptomics to explore the expression, prognosis, and mutation status of genes related to disulfidptosis. Using the LUAD multi- -omics cohorts in the TCGA database, we explore the molecular characteristics of subtypes related to disulfidptosis. Employing various machine learning algorithms, we construct a robust prognostic model to predict immune therapy responses and explore the model's impact on the tumor microenvironment through single-cell transcriptome data. Finally, the biological functions of genes related to the prognostic model are verified through laboratory experiments. <p> Results: Genes related to disulfidptosis exhibit high expression and significant prognostic value in various cancers, including LUAD. Two disulfidptosis subtypes with distinct prognoses and molecular characteristics have been identified, leading to the development of a robust DSRS prognostic model, where a lower risk score correlates with a higher response rate to immunotherapy and a better patient prognosis. NAPSA, a critical gene in the risk model, was found to inhibit the proliferation and migration of LUAD cells. <p> Conclusion: Our research introduces an innovative prognostic risk model predicated upon disulfidptosis genes for patients afflicted with Lung Adenocarcinoma (LUAD). This model proficiently forecasts the survival rates and therapeutic outcomes for LUAD patients, thereby delineating the high-risk population with distinctive immune cell infiltration and a state of immunosuppression. Furthermore, NAPSA can inhibit the proliferation and invasion capabilities of LUAD cells, thereby identifying new molecules for clinical targeted therapy.</p>]]></description> </item><item><title><![CDATA[Revolutionizing Neurological Disorder Treatment: Integrating Innovations in
Pharmaceutical Interventions and Advanced Therapeutic Technologies]]></title><link>https://www.benthamscience.comarticle/139669</link><description><![CDATA[Neurological disorders impose a significant burden on individuals, leading to disabilities and a reduced quality of life. However, recent years have witnessed remarkable advancements in pharmaceutical interventions aimed at treating these disorders. This review article aims to provide an overview of the latest innovations and breakthroughs in neurological disorder treatment, with a specific focus on key therapeutic areas such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, and stroke. This review explores emerging trends in drug development, including the identification of novel therapeutic targets, the development of innovative drug delivery systems, and the application of personalized medicine approaches. Furthermore, it highlights the integration of advanced therapeutic technologies such as gene therapy, optogenetics, and neurostimulation techniques. These technologies hold promise for precise modulation of neural circuits, restoration of neuronal function, and even disease modification. While these advancements offer hopeful prospects for more effective and tailored treatments, challenges such as the need for improved diagnostic tools, identification of new targets for intervention, and optimization of drug delivery methods will remain. By addressing these challenges and continuing to invest in research and collaboration, we can revolutionize the treatment of neurological disorders and significantly enhance the lives of those affected by these conditions.]]></description> </item><item><title><![CDATA[Deubiquitylase USP31 Induces Autophagy and Promotes the Progression
in Lung Squamous Cell Carcinoma Cells by Stabilizing E2F1 Expression]]></title><link>https://www.benthamscience.comarticle/137088</link><description><![CDATA[<P>Background: Autophagy exerts a vital role in the progression of lung squamous cell carcinoma (LUSC). Ubiquitin-specific peptidase 31 (USP31) has recently been found to be involved in the development of a variety of cancers. However, whether USP31 modulates autophagy in LUSC remains unclear. <P> Methods: This study revealed that high levels of USP31 were discovered in LUSC tissue samples employing the Gene Expression Profiling Interactive Analysis (GEPIA) database, quantitative real- time PCR (qRT-PCR), and Western blot analysis. Cell proliferation was tested <i>via</i> cell counting kit 8 (CCK-8) as well as colony formation, demonstrating that USP31-stable knockdown reduced cell viability. <P> Results: Immunofluorescence analysis illustrated that USP31 knockdown blocked the occurrence of LUSC autophagy. Meanwhile, USP31 has been shown to stabilize the expression of E2F transcription factor 1 (E2F1) through the proteasome pathway. Furthermore, overexpressed E2F1 effectively eliminated the effect of USP31 knockdown on LUSC cell proliferation and autophagy. <P> Conclusion: In summary, this investigation proved that USP31 promoted LUSC cell growth and autophagy, at least in part by stabilizing E2F1 expression, which provided a potential therapeutic gene for the treatment of LUSC.</P>]]></description> </item><item><title><![CDATA[ZIP14 Affects the Proliferation, Apoptosis, and Migration of Cervical
Cancer Cells by Regulating the P38 MAPK Pathway]]></title><link>https://www.benthamscience.comarticle/136206</link><description><![CDATA[<p>Background: Cervical cancer (CC) remains a major public health concern and is a leading cause of female mortality worldwide. Understanding the molecular basis of its pathogenesis is essential for the development of novel therapeutic strategies. In this study, we aimed to dissect the role of a specific molecule, ZIP14, in the initiation and progression of CC. <p> Methods: We used Gene Expression Omnibus for target gene identification, while KEGG was used to delineate CC-related pathways. Proliferation, migration, and apoptosis levels in CC cells were assessed using CCK8, Transwell, and flow cytometry, respectively. The effect of the target genes on the <i>in vivo</i> tumorigenesis of CC cells was evaluated using the subcutaneous tumorigenesis assay. <p> Results: ZIP14 (SLC39A14) was found to be underexpressed in CC samples. Our KEGG pathway analysis revealed the potential involvement of the P38 mitogen-activated protein kinase (MAPK) pathway in CC pathogenesis. Overexpression of ZIP14 in HeLa and Caski cells increased p38 phosphorylation, inhibited cell growth and migration, and enhanced apoptosis. Conversely, ZIP14 knockdown produced the opposite effects. Importantly, the bioeffects induced by ZIP14 overexpression could be counteracted by the p38 MAPK pathway inhibitor SB203580. <i>In vivo</i> experiments further confirmed the influence of ZIP14 on CC cell migration. <p> Conclusion: Our study is the first to elucidate the pivotal role of ZIP14 in the pathogenesis of CC, revealing its inhibitory effects through the activation of the p38 MAPK signaling pathway. The discovery not only provides a deeper understanding of CC's molecular underpinnings, but also highlights ZIP14 as a promising therapeutic target. As ZIP14 holds significant potential for therapeutic interventions, our findings lay a robust foundation for further studies and pave the way for the exploration of novel treatment modalities for cervical cancer.</p>]]></description> </item><item><title><![CDATA[Targeted Inhibition of the PI3K/Akt/mTOR Signaling Axis: Potential for
Sarcoma Therapy]]></title><link>https://www.benthamscience.comarticle/137681</link><description><![CDATA[Sarcoma is a heterogeneous group of malignancies often resistant to conventional chemotherapy and radiation therapy. The phosphatidylinositol-3-kinase/ protein kinase B /mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway has emerged as a critical cancer target due to its central role in regulating key cellular processes such as cell growth, proliferation, survival, and metabolism. Dysregulation of this pathway has been implicated in the development and progression of bone sarcomas (BS) and soft tissue sarcomas (STS). PI3K/Akt/mTOR inhibitors have shown promising preclinical and clinical activity in various cancers. These agents can inhibit the activation of PI3K, Akt, and mTOR, thereby reducing the downstream signaling events that promote tumor growth and survival. In addition, PI3K/Akt/mTOR inhibitors have been shown to enhance the efficacy of other anticancer therapies, such as chemotherapy and radiation therapy. The different types of PI3K/Akt/mTOR inhibitors vary in their specificity, potency, and side effect profiles and may be effective depending on the specific sarcoma type and stage. The molecular targeting of PI3K/Akt/mToR pathway using drugs, phytochemicals, nanomaterials (NMs), and microbe-derived molecules as Pan-PI3K inhibitors, selective PI3K inhibitors, and dual PI3K/mTOR inhibitors have been delineated. While there are still challenges to be addressed, the preclinical and clinical evidence suggests that these inhibitors may significantly improve patient outcomes. Further research is needed to understand the potential of these inhibitors as sarcoma therapeutics and to continue developing more selective and effective agents to meet the clinical needs of sarcoma patients.]]></description> </item><item><title><![CDATA[Targeted Mevalonate Pathway and Autophagy in Antitumor
Immunotherapy]]></title><link>https://www.benthamscience.comarticle/137825</link><description><![CDATA[Tumors of the digestive system are currently one of the leading causes of cancer-related death worldwide. Despite considerable progress in tumor immunotherapy, the prognosis for most patients remains poor. In the tumor microenvironment (TME), tumor cells attain immune escape through immune editing and acquire immune tolerance. The mevalonate pathway and autophagy play important roles in cancer biology, antitumor immunity, and regulation of the TME. In addition, there is metabolic crosstalk between the two pathways. However, their role in promoting immune tolerance in digestive system tumors has not previously been summarized. Therefore, this review focuses on the cancer biology of the mevalonate pathway and autophagy, the regulation of the TME, metabolic crosstalk between the pathways, and the evaluation of their efficacy as targeted inhibitors in clinical tumor immunotherapy.]]></description> </item><item><title><![CDATA[Elucidating the Role of Pro-renin Receptors in Pancreatic Ductal
Adenocarcinoma Progression: A Novel Therapeutic Target in Cancer
Therapy]]></title><link>https://www.benthamscience.comarticle/137872</link><description><![CDATA[Pancreatic cancer is a highly aggressive malignancy with a very poor prognosis. The 5- year survival in these patients is very low, and most patients develop drug resistance to current therapies, so additional studies are needed to identify the potential role of new drug targets for the treatment of pancreatic cancer. Recent investigations have been performed regarding the roles of pro-renin receptors (PRR) in the initiation and development of cancers. PRR is a component of the local renin-angiotensin system (RAS). Local tissue RAS has been known in diverse organ systems, including the pancreas. Various investigations have implicated that PRRs are associated with the upregulation of various signaling pathways, like the renin-angiotensin system pathway, PI3K/Akt/mTOR, and the Wnt-signaling pathways, to contribute to pathological conditions, including cancer. In this review, we presented an overview of the role of PRR in the progression of pancreatic adenocarcinoma.]]></description> </item><item><title><![CDATA[Proteomic Analysis of the Molecular Mechanisms of Chlorpromazine
Inhibiting Migration of Oral Squamous Cell Carcinoma]]></title><link>https://www.benthamscience.comarticle/138681</link><description><![CDATA[<p>Background: Oral squamous cell carcinoma (OSCC) is a common malignant tumor of the head and neck region known for its high metastatic and invasive potential. Chlorpromazine (CPZ) has been shown to inhibit the growth of oral cancer cells. However, the effects of CPZ on OSCC migration and its underlying molecular mechanisms remain unclear. <p> Objectives: We aimed to identify global protein changes and potential core proteins involved in CPZ-mediated inhibition of migration in SCC-15 cells using proteomics. <p> Methods: We assessed the effect of CPZ on SCC-15 using CCK-8 assays and wound healing experiments. Next, we performed LC-MS-based proteomic analysis to identify protein alterations in SCC-15 cells treated with CPZ at different times. Differential expression proteins (DEPs) were identified and subjected to bioinformatics analysis using GO, KEGG, and PPI tools. Key candidate proteins were selected and validated using the TCGA-HNSCC database and molecular docking. <p> Results: It was found that 20μm of CPZ had no effect on cell proliferation, but inhibited cell migration. A total of 4748 proteins were identified by Proteomics, among which 56 DEPs were identified, including 34 upregulated proteins and 22 downregulated proteins. Three proteins (RPF2, ACTB, and TGFBI) were identified as key candidate proteins associated with cell adhesion and migration in oral cancer cells. <p> Conclusion: CPZ may affect the expression of RPF2, ACTB, and TGFBI proteins and change the extracellular matrix and cell adhesion function, thus inhibiting the migration of SCC-15 cells. The results of this study provide a robust basis for further research on the molecular mechanism of CPZ to inhibit the migration of OSCC.</p>]]></description> </item><item><title><![CDATA[Synthesis, DPPH Radical Scavenging, Cytotoxic Activity, and Apoptosis
Induction Efficacy of Novel Thiazoles and Bis-thiazoles]]></title><link>https://www.benthamscience.comarticle/135849</link><description><![CDATA[<p>Background: Heterocyclic materials-containing thiazoles exhibited incredible importance in pharmaceutical chemistry and drug design due to their extensive biological properties. <p> Methods: Synthesis of thiazoles and bis-thiazoles from the reaction of 2-((6-Nitrobenzo[ d][1,3]dioxol-5-yl)methylene)hydrazine-1-carbothioamide with hydrazonoyl chlorides in dioxane and in the existence of triethylamine as basic catalyst. The antioxidant, <i>in vitro</i> antiproliferative, and cytotoxicity efficacy of thiazoles and bis-thiazoles were measured. <p> Results: In this work, novel series of 5-methyl-2-(2-(-(6-nitrobenzo[d][1,3]dioxol-5-yl)methylene) hydrazinyl)-4-(aryldiazenyl)thiazoles (4a-f) were prepared <i>via</i> the reaction of hydrazonoyl chlorides 2a-f with 2-((6-nitrobenzo[d][1,3]dioxol-5-yl)methylene)hydrazine-1-carbothioamide (1) in dioxane and employing triethylamine as basic catalyst. Following the same procedure, bisthiazoles (6, 8, and 10) have been synthesized by utilizing bis-hydrazonoyl chlorides (5, 7, and 9) and carbothioamide 1 in a molar ratio (1:2), respectively. The distinctive features in the structure of isolated products were elucidated by spectroscopic tools and elemental analyses. The antioxidant, in vitro anti-proliferative, cytotoxicity, and anti-cancer efficacy of thiazoles and bis-thiazoles were evaluated. Compounds 4d and 4f were the most potent antioxidant agents. Gene expression of apoptosis markers and fragmentation assay of DNA were assessed to explore the biochemical mechanism of synthesized products. Thiazoles significantly inhibited cell growth and proliferation more than bis-thiazoles. They induced apoptosis through induction of apoptotic gene expression P53 and downregulation of antiapoptotic gene expression Bcl-2. Moreover, they induced fragmentation of DNA in cancer cells, indicating that they could be employed as anticancer agents by inhibiting tumor growth and progression and can be considered effective compounds in the strategy of anti-cancer agents’ discovery. <p> Conclusion: Synthesis, DPPH Radical Scavenging, Cytotoxic activity, and Apoptosis Induction Efficacy based on Novel Thiazoles and Bis-thiazoles.</p>]]></description> </item><item><title><![CDATA[Ramifications of m6A Modification on ncRNAs in Cancer]]></title><link>https://www.benthamscience.comarticle/139672</link><description><![CDATA[N6-methyladenosine (m6A) is an RNA modification wherein the N6-position of adenosine is methylated. It is one of the most prevalent internal modifications of RNA and regulates various aspects of RNA metabolism. M6A is deposited by m6A methyltransferases, removed by m6A demethylases, and recognized by reader proteins, which modulate splicing, export, translation, and stability of the modified mRNA. Recent evidence suggests that various classes of noncoding RNAs (ncRNAs), including microRNAs (miRNAs), circular RNAs (circRNAs), and long con-coding RNAs (lncRNAs), are also targeted by this modification. Depending on the ncRNA species, m6A may affect the processing, stability, or localization of these molecules. The m6Amodified ncRNAs are implicated in a number of diseases, including cancer. In this review, the author summarizes the role of m<sup>6</sup>A modification in the regulation and functions of ncRNAs in tumor development. Moreover, the potential applications in cancer prognosis and therapeutics are discussed.]]></description> </item><item><title><![CDATA[Antiobesity Drug Discovery Research: <i>In vitro</i> Models for Shortening the
Drug Discovery Pipeline]]></title><link>https://www.benthamscience.comarticle/139247</link><description><![CDATA[Obesity is a growing global health problem, leading to various chronic diseases. Despite standard treatment options, the prevalence of obesity continues to rise, emphasizing the need for new drugs. <i>in vitro</i> methods of drug discovery research provide a time and cost-saving platform to identify new antiobesity drugs. The review covers various aspects of obesity and drug discovery research using <i>in vitro</i> models. Besides discussing causes, diagnosis, prevention, and treatment, the review focuses on the advantages and limitations of <i>in vitro</i> studies and exhaustively covers models based on enzymes and cell lines from different animal species and humans. In contrast to conventional in vivo animal investigations, <i>in vitro</i> preclinical tests using enzyme- and cell line-based assays provide several advantages in development of antiobesity drugs. These methods are quick, affordable, and provide high-throughput screening. They can also yield insightful information about drug-target interactions, modes of action, and toxicity profiles. By shedding light on the factors that lead to obesity, <i>in vitro</i> tests can also present a chance for personalized therapy. Technology will continue to evolve, leading to the creation of more precise and trustworthy <i>in vitro</i> assays, which will become more and more crucial in the search for novel antiobesity medications.]]></description> </item><item><title><![CDATA[Tetrandrine for Targeting Therapy Resistance in Cancer]]></title><link>https://www.benthamscience.comarticle/138963</link><description><![CDATA[During the last five decades, there has been tremendous development in our understanding of cancer biology and the development of new and novel therapeutics to target cancer. However, despite these advances, cancer remains the second leading cause of death across the globe. Most cancer deaths are attributed to the development of resistance to current therapies. There is an urgent and unmet need to address cancer therapy resistance. Tetrandrine, a bis-benzyl iso-quinoline, has shown a promising role as an anti-cancer agent. Recent work from our laboratory and others suggests that tetrandrine and its derivatives could be an excellent adjuvant to the current arsenal of anti-cancer drugs. Herein, we provide an overview of resistance mechanisms to current therapeutics and review the existing literature on the anti-cancer effects of tetrandrine and its potential use for overcoming therapy resistance in cancer.]]></description> </item><item><title><![CDATA[ZNF695, A Potential Prognostic Biomarker, Correlates with Im mune
Infiltrates in Cervical Squamous Cell Carcinoma and Endoce rvical
Adenocarcinoma: Bioinformatic Analysis and Experimental Verification]]></title><link>https://www.benthamscience.comarticle/138901</link><description><![CDATA[<p>Background: The role of Zinc Finger Protein 695 (ZNF695) is unclear in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). <p> Objective: The objective of this study was to conduct a comprehensive analysis and experimental validation of ZNF695 in CESC. <p> Methods: The study investigated the expression of ZNF695 in both pan-cancer and CESC, utilizing data from The Cancer Genome Atlas (TCGA) database to assess its diagnostic value. The present study investigated the association between ZNF695 expression levels and clinical characteristics, as well as prognosis, in patients with CESC. The study explored potential regulatory networks involving ZNF695, including its association with immune infiltration, immune score, stemness index based on mRNA expression (mRNAsi), and drug sensitivity in CESC. We explored the expression of ZNF695 in CESC single cells. ZNF695 expression was validated using GSE29570. <p> Results: ZNF695 was found to be aberrantly expressed in pan-cancer and CESC. There was a significant correlation observed between an elevated level of ZNF695 expression in patients with CESC and histological grade (p = 0.017). Furthermore, a strong association was found between high ZNF695 expression in CESC patients and poorer overall survival (OS) (HR: 1.87; 95% CI: 1.17-3.00; p = 0.009), Progression-free Survival (PFS) (HR: 1.86; 95% CI: 1.16-2.98; p = 0.010), and Disease-specific Survival (DSS) (HR: 1.98; 95% CI: 1.15-3.42; p = 0.014). The expression of ZNF695 in CESC patients (p = 0.006) was identified as an independent prognostic determinant. ZNF695 was associated with steroid hormone biosynthesis, oxidative phosphorylation, and so on. ZNF695 expression correlated with immune infiltration, immune score, and mRNAsi in CESC. ZNF695 expression significantly and negatively correlated with AICA ribonucleotide, BIX02189, QL-XI-92, STF-62247, and SNX-2112 in CESC. ZNF695 gene was upregulated in CESC tissues and cell lines. ZNF695 was significantly upregulated in the CESC cell lines. <p> Conclusion: ZNF695 may be a potential prognostic biomarker and immunotherapeutic target for CESC patients.</p>]]></description> </item><item><title><![CDATA[PaSTe. Blockade of the Lipid Phenotype of Prostate Cancer as
Metabolic Therapy: A Theoretical Proposal]]></title><link>https://www.benthamscience.comarticle/132354</link><description><![CDATA[<p>Background: Prostate cancer is the most frequently diagnosed malignancy in 112 countries and is the leading cause of death in eighteen. In addition to continuing research on prevention and early diagnosis, improving treatments and making them more affordable is imperative. In this sense, the therapeutic repurposing of low-cost and widely available drugs could reduce global mortality from this disease. The malignant metabolic phenotype is becoming increasingly important due to its therapeutic implications. Cancer generally is characterized by hyperactivation of glycolysis, glutaminolysis, and fatty acid synthesis. However, prostate cancer is particularly lipidic; it exhibits increased activity in the pathways for synthesizing fatty acids, cholesterol, and fatty acid oxidation (FAO). <p> Objective: Based on a literature review, we propose the PaSTe regimen (Pantoprazole, Simvastatin, Trimetazidine) as a metabolic therapy for prostate cancer. Pantoprazole and simvastatin inhibit the enzymes fatty acid synthase (FASN) and 3-hydroxy-3-methylglutaryl- coenzyme A reductase (HMGCR), therefore, blocking the synthesis of fatty acids and cholesterol, respectively. In contrast, trimetazidine inhibits the enzyme 3-&#946;-Ketoacyl- CoA thiolase (3-KAT), an enzyme that catalyzes the oxidation of fatty acids (FAO). It is known that the pharmacological or genetic depletion of any of these enzymes has antitumor effects in prostatic cancer. <p> Results: Based on this information, we hypothesize that the PaSTe regimen will have increased antitumor effects and may impede the metabolic reprogramming shift. Existing knowledge shows that enzyme inhibition occurs at molar concentrations achieved in plasma at standard doses of these drugs. <p> Conclusion: We conclude that this regimen deserves to be preclinically evaluated because of its clinical potential for the treatment of prostate cancer.</p>]]></description> </item><item><title><![CDATA[The Therapeutic Application of Hydrogen in Cancer: The Potential and
Challenges]]></title><link>https://www.benthamscience.comarticle/139804</link><description><![CDATA[Hydrogen therapy has emerged as a possible approach for both preventing and treating cancer. Cancers are often associated with oxidative stress and chronic inflammation. Hydrogen, with its unique physiological functions and characteristics, exhibits antioxidant, anti-inflammatory, and anti-apoptotic properties, making it an attractive candidate for cancer treatment. Through its ability to mitigate oxidative damage, modulate inflammatory responses, and sustain cellular viability, hydrogen demonstrates significant potential in preventing cancer recurrence and improving treatment outcomes. Preclinical studies have shown the efficacy of hydrogen therapy in several cancer types, highlighting its ability to enhance the effectiveness of conventional treatments while reducing associated side effects. Furthermore, hydrogen therapy has been found to be safe and well-tolerated in clinical settings. Nonetheless, additional investigations are necessary to improve a comprehensive understanding of the mechanisms underlying hydrogen's therapeutic potential and refine the administration and dosage protocols. However, further clinical trials are still needed to explore its safety profile and capacity. In aggregate, hydrogen therapy represents an innovative and promising treatment for several malignancies.]]></description> </item><item><title><![CDATA[Mechanism Research of PZD Inhibiting Lung Cancer Cell Proliferation, Invasion,
and Migration based on Network Pharmacology]]></title><link>https://www.benthamscience.comarticle/139545</link><description><![CDATA[<P> Background: A classic Chinese medicine decoction, <i>Pinellia ternata</i> (Thunb.) Breit.-<i>Zingiber officinale</i> Roscoe (Ban-Xia and Sheng-Jiang in Chinese) decoction (PZD), has shown significant therapeutic effects on lung cancer. <P> Objective: This study aimed to explore and elucidate the mechanism of action of PZD on lung cancer using network pharmacology methods. <P> Methods: Active compounds were selected according to the ADME parameters recorded in the TCMSP database. Potential pathways related to genes were identified through GO and KEGG analysis. The compoundtarget network was constructed by using Cytoscape 3.7.1 software, and the core common targets were obtained by protein-protein interaction (PPI) network analysis. Batch molecular docking of small molecule compounds and target proteins was carried out by using the AutoDock Vina program. Different concentrations of PZD water extracts (10, 20, 40, 80, and 160 μg/mL) were used on lung cancer cells. Moreover, MTT and Transwell experiments were conducted to validate the prominent therapeutic effects of PZD on lung cancer cell H1299. <P> Results: A total of 381 components in PZD were screened, of which 16 were selected as bioactive compounds. The compound-target network consisting of 16 compounds and 79 common core targets was constructed. MTT experiment showed that the PZD extract could inhibit the cell proliferation of NCI-H1299 cells, and the IC<sub>50</sub> was calculated as 97.34 ± 6.14 μg/mL. Transwell and wound-healing experiments showed that the PZD could significantly decrease cell migration and invasion at concentrations of 80 and 160 μg/mL, respectively. The <i>in vitro</i> experiments confirmed that PZD had significant therapeutic effects on lung cancer cells, mainly through the PI3K/AKT signaling pathway. <P> Conclusion: PZD could inhibit the cell proliferation, migration, and invasion of NCI-H1299 cells partially through the PI3K/AKT signaling pathway. These findings suggested that PZD might be a potential treatment strategy for lung cancer patients.</P>]]></description> </item><item><title><![CDATA[The Impact of HAPPY (Humanity Assurance Protocol in Interventional
Radiotherapy) on the Psychological Well-being of Gynecological Cancer
Patients]]></title><link>https://www.benthamscience.comarticle/134741</link><description><![CDATA[<P>Background: HAPPY (Humanity Assurance Protocol in Interventional Radiotherapy) reports the necessity for gynecological cancer patients to undergo interventional radiotherapy (IRT, also called brachytherapy). The present paper has evaluated how some precautions may improve the psychological well-being of the patients during IRT. <P> Methods: Patients with gynecological cancer undergoing IRT-HDR were analyzed. Patients answered three questionnaires before the IRT procedure (T0) and at the end of IRT (T1): Distress Thermometer (DT), Numerical Rating Scale for IRT procedure distress (NRS), and Hospital Anxiety and Depression Scale (HADS). Correlations have been calculated pairwise through pandas. corrwith with a Pearson algorithm, and the p-values have been calculated through scipy.stats.pearsonr. Plots have been generated through seaborn and matplotlib. A Wilcoxon test was used. <P> Results: 55 patients were selected for this study. The median age of the patients was 64 (range, 39-84) years. 52 patients were with stage I endometrial cancer, whereas 3/3 patients with cervical cancer had locally advanced stages (IIB-IVA). 26 patients had a high education level (47.3%), and 38 were married or with a partner (69.1%). Only 14/55 (25.45%) patients were working. The HADS, DT, and NRS averages before the IRT procedure (T0) were 10.2, 3.8, and 4.3, respectively. After applying the HAPPY protocol, the HADS, DT, and NRS averages after IRT (T1) were 9.4, 3.4, and 2.6, respectively. The Wilcoxon signed rank test analysis showed a significant improvement in NRS (p < 0.00001) and HADS (p = 0.034). Living with a partner, parents or relatives was the only parameter statistically significantly associated with better DT pre-IRT (p = 0.04), HADS pre-IRT (p = 0.01), DT post-IRT (p = 0.01), and HADS post-IRT (p = 0.04). <P> Conclusion: In our study, the HAPPY protocol was associated with a significant reduction in patients’ distress, anxiety, and discomfort.</P>]]></description> </item><item><title><![CDATA[Curcuminoids as Cell Signaling Pathway Modulators: A Potential
Strategy for Cancer Prevention]]></title><link>https://www.benthamscience.comarticle/133477</link><description><![CDATA[Despite substantial advancements in curative modern medicine in the last few decades, cancer risk and casualty rates have continued to mount globally. The exact reason for cancer's onset and progression is still unknown. However, skeletal and functional abnormalities in the genetic code are assumed to be the primary cause of cancer. Many lines of evidence reported that some medicinal plants can be utilized to curb cancer cell proliferation with a safe, fruitful, and cost-efficient perspective. Curcuminoid, isolated from <i>Curcuma longa</i>, have gotten a lot of focus due to their anticancer potential as they reduce tumor progression, invasion, and dissemination. Further, they modulated signal transduction routes like MAPK, PI3K/Akt/mTOR, JAK/STAT, and Wnt/&#946;-catenin, etc., and triggered apoptosis as well as actuated autophagy in malignant cells without altering the normal cells, thus preventing cancer progression. Besides, Curcuminoid also regulate the function and expression of anti-tumor and carcinogenic miRNAs. Clinical studies also reported the therapeutic effect of Curcuminoid against various cancer through decreasing specific biomarkers like TNF-&#945;, Bcl-2, COX-2, PGE2, VEGF, I&#954;K&#946;, and various cytokines like IL-12p70, IL-10, IL-2, IFN-&#947; levels and increasing in p53 and Bax levels. Thus, in the present review, we abridged the modulation of several signal transduction routes by Curcuminoids in various malignancies, and its modulatory role in the initiation of tumor-suppressive miRNAs and suppression of the oncogenic miRNAs are explored. Additionally, various pharmacokinetic approaches have been projected to address the Curcuminoids bioavailability like the use of piperine as an adjuvant; nanotechnology- based Curcuminoids preparations utilizing Curcuminoids analogues are also discussed.]]></description> </item><item><title><![CDATA[SETD1A-mediated Methylation of H3K4me3 Inhibits Ferroptosis in
Non-small Cell Lung Cancer by Regulating the WTAPP1/WTAP Axis]]></title><link>https://www.benthamscience.comarticle/132075</link><description><![CDATA[<p>Introduction: SETD1A is upregulated in non-small cell lung cancer (NSCLC) tissues. This study investigated the molecular mechanism of the SETD1A/WTAPP1/WTAP axis in NSCLC. <p> Methods: Ferroptosis is a unique cell death mode driven by iron-reliant phospholipid peroxidation, which is regulated by multiple cellular metabolic pathways, including REDOX homeostasis, iron metabolism, mitochondrial activity and metabolism of amino acids, lipids and sugars. Thus, the levels of ferroptosis markers (MDA, SOD, GSH) were measured <i>in vitro</i>, and NSCLC cell behaviors were assessed. SETD1A-mediated H3K4me3 methylation was analyzed. SETD1A-exerted effects on ferroptosis and tumor growth in vivo were verified in nude mouse models. <p> Results: SETD1A was highly expressed in NSCLC cells. Silencing SETD1A suppressed NSCLC cell proliferation and migration, inhibited MDA, and enhanced GPX4, SOD, and GSH levels. SETD1A elevated WTAP expression through WTAPP1 upregulation by mediating H3K4me3 methylation in the WTAPP1 promoter region. WTAPP1 overexpression partly averted the promotional effect of silencing SETD1A on NSCLC cell ferroptosis. WTAP interference abrogated the inhibitory effects of WTAPP1 on NSCLC cell ferroptosis. Silencing SETD1A facilitated ferroptosis and accelerated tumor growth in nude mice through the WTAPP1/WTAP axis. <p> Conclusion: SETD1A amplified WTAP expression through WTAPP1 upregulation by mediating H3K4me3 modification in the WTAPP1 promoter region, thus promoting NSCLC cell proliferation and migration and inhibiting ferroptosis.</p>]]></description> </item><item><title><![CDATA[Recent Advances on PKM2 Inhibitors and Activators in Cancer
Applications]]></title><link>https://www.benthamscience.comarticle/132912</link><description><![CDATA[Metabolic reprogramming of cells, from the normal mode of glucose metabolism named glycolysis, is a pivotal characteristic of impending cancerous cells. Pyruvate kinase M2 (PKM2), an important enzyme that catalyzes the final rate-limiting stage during glycolysis, is highly expressed in numerous types of tumors and aids in development of favorable conditions for the survival of tumor cells. Increasing evidence has suggested that PKM2 is one of promising targets for innovative drug discovery, especially for the developments of antitumor therapeutics. Herein, we systematically summarize the recent advancement on PKM2 modulators including inhibitors and activators in cancer applications. We also discussed the classifications of pyruvate kinases in mammals and the biological functions of PKM2 in this review. We do hope that this review would provide a comprehensive understanding of the current research on PKM2 modulators, which may benefit the development of more potent PKM2-related drug candidates to treat PKM2-associated diseases including cancers in future.]]></description> </item><item><title><![CDATA[The Application of Nanotechnological Therapeutic Platforms against
Gynecological Cancers]]></title><link>https://www.benthamscience.comarticle/139240</link><description><![CDATA[Gynecological cancers (GCs), ovarian, cervical, and endometrial/uterine cancers, are often associated with poor outcomes. Despite the development of several therapeutic modalities against GCs, the effectiveness of the current therapeutic approaches is limited due to their side effects, low therapeutic index, short halflife, and resistance to therapy. To overcome these limitations, nano delivery-based approaches have been introduced with the potential of targeted delivery, reduced toxicity, controlled release, and improved bioavailability of various cargos. This review summarizes the application of different nanoplatforms, such as lipid-based, metal- based, and polymeric nanoparticles, to improve the chemo/radio treatments of GC. In the following work, the use of nanoformulated agents to fight GCs has been mentioned in various clinical trials. Although nanosystems have their own challenges, the knowledge highlighted in this article could provide deep insight into translations of NPs approaches to overcome GCs.]]></description> </item><item><title><![CDATA[Bioinformatics and Experimental Study Revealed LINC00982/
miR-183-5p/ABCA8 Axis Suppresses LUAD Progression]]></title><link>https://www.benthamscience.comarticle/136227</link><description><![CDATA[<p>Background: Lung adenocarcinoma (LUAD) is a major health challenge worldwide with an undesirable prognosis. LINC00982 has been implicated as a tumor suppressor in diverse human cancers; however, its role in LUAD has not been fully characterized. <p> Methods: Expression level and prognostic value of LINC00982 were investigated in pan-cancer and lung cancer from The Cancer Genome Atlas (TCGA) project. Differential expression analysis based on the LINC00982 expression level was performed in LUAD followed by gene set enrichment analysis (GSEA) and functional enrichment analyses. The association between LINC00982 expression and tumor immune microenvironment characteristics was evaluated. A potential ceRNA regulatory axis was identified and experimentally validated. <p> Results: We found that LINC00982 expression was downregulated and correlated with poor prognosis in LUAD. Enrichment analyses revealed that LINC00982 could inhibit DNA damage repair and cell proliferation, but enhance tumor metabolic reprogramming. We identified a competing endogenous RNA network involving LINC00982, miR-183-5p, and ATP-binding cassette subfamily A member 8 (ABCA8). Luciferase assays confirmed that miR-183-5p can interact with LINC00982 and ABCA8. Forced miR-183-5p expression reduced LINC00982 transcript levels and suppressed ABCA8 expression. <p> Conclusions: Our findings revealed the LINC00982/miR-183-5p/ABCA8 axis as a potential therapeutic target in LUAD.</p>]]></description> </item><item><title><![CDATA[Current and Emerging Pharmacological Therapies for Cushing's Disease]]></title><link>https://www.benthamscience.comarticle/138844</link><description><![CDATA[Cushing’s Disease (CD), hypercortisolism due to pituitary ACTH secreting neuroendocrine neoplasm, is associated with increased morbidity and, if untreated, mortality in about half of the affected individuals. Consequently, the timely initiation of effective treatment is mandatory. Neurosurgery is the first line and the only potentially curative treatment; however, 30% of patients will have persistent disease post-surgery. Furthermore, a small percentage of those initially controlled will develop hypercortisolism during long-term follow- up. Therefore, patients with persistent or recurrent disease, as well as those considered non-eligible for surgery, will need a second-line therapeutic approach, i.e., pharmacotherapy. Radiation therapy is reserved as a third-line therapeutic option due to its slower onset of action and its unfavorable profile regarding complications. During the past few years, the understanding of molecular mechanisms implicated in the physiology of the hypothalamus-pituitary-adrenal axis has evolved, and new therapeutic targets for CD have emerged. In the present review, currently available treatments, compounds currently tested in ongoing clinical trials, and interesting, potentially new targets emerging from unraveling molecular mechanisms involved in the pathophysiology of Cushing’s disease are discussed.]]></description> </item><item><title><![CDATA[Network Pharmacology Analysis on the Mechanism of Xihuangwan in Treating
Rectal Cancer and Radiation Enteritis]]></title><link>https://www.benthamscience.comarticle/138616</link><description><![CDATA[<P>Background: Recent studies have shown that XihuangWan (XHW) is a kind of Chinese medicine with significant anti-tumor and anti-inflammatory activities. However, its mechanism for preventing and treating radiation proctitis in rectal cancer patients during radiotherapy remains unclear. <P> Methods: This study employed the network pharmacology to establish a “drug-active ingredient-target genedisease” network via using TCMSP, SymMap, GeneCard, and OMIM databases. The PPI network was conducted by the String tool. The core targets of XHW in the treatment of rectal cancer and radiation enteritis were identified by topological analysis, and the functional annotation analysis and pathway enrichment analysis were performed. <P> Results: A total of 61 active ingredients of XHW ingredients, 4607 rectal cancer-related genes, 5803 radiation enteritis-related genes, and 68 common targets of XHW in the treatment of rectal cancer and radiation enteritis were obtained. PTGS1 and NR3C2, as identified potential targets, were significantly associated with OS of colorectal cancer patients. GO and KEGG enrichment analysis showed that bioinformatics annotation of these common genes was mainly involved in DNA-binding transcription factor, PI3K/Akt, TNF, HIF-1 signaling pathway, and colorectal cancer pathway. <P> Conclusion: The active ingredients of XHW, mainly including Quercetin, Ellagic acid, and Stigmasterol, might act on common targets of rectal cancer and radiation enteritis, such as PTGS1, NR3C2, IL-6, EGFR, HIF-1A, CASP3, BCL2, ESR1, MYC, and PPARG, and regulate multiple signaling pathways like PI3K-Akt, TNF, and HIF-1 to inhibit tumor proliferation, tumor angiogenesis, inflammatory responses, and oxidative stress, thereby achieving prevention and treatment of radiation enteritis in rectal cancer patients during radiotherapy. It provided an important reference for further elucidating the anti-inflammation and anti-tumor mechanism and clinical application of XHW.</P>]]></description> </item><item><title><![CDATA[Roles of AFAP1-AS1 in Gynecology and Urogenital System]]></title><link>https://www.benthamscience.comarticle/138441</link><description><![CDATA[<p>Background: Human disease onset and progression are strongly associated with aberrant long noncoding RNA (lncRNA) expression, highlighting the functional regulatory role of lncRNA. Actin filament-associated protein 1-antisense RNA 1 (AFAP1-AS1), a member of lncRNAs, is located on the antisense strand of Actin filament-associated protein 1 (AFAP1). <p> Methods: We conducted a comprehensive review of AFAP1-AS1's functions in gynecology and urogenital systems using the “PubMed” database. <p> Results: Our analysis reveals that AFAP1-AS1 is overexpressed and engages in the initiation and process of gynecological and urogenital diseases. The regulatory mechanisms employed by AFAP1-AS1 involve four major strategies: gene-level effects, competition for microRNA (miRNA) repression, protein binding, participation in signaling networks that influence cellular processes such as proliferative phenotype, migration, invasiveness, epithelial-mesenchymal transition (EMT), cycle regulation, drug resistance, and more. Furthermore, AFAP1-AS1 is implicated in guiding clinicopathological characteristics. <p> Conclusion: AFAP1-AS1 holds promise as a potent diagnostics and treatment option for gynecological and genitourinary systems in the future.]]></description> </item><item><title><![CDATA[Interplay between LncRNA/miRNA and TGF-&#946; Signaling in the Tumorigenesis
of Gynecological Cancer]]></title><link>https://www.benthamscience.comarticle/138262</link><description><![CDATA[Gynecologic cancers are among the most common malignancies with aggressive features and poor prognosis. Tumorigenesis in gynecologic cancers is a complicated process that is influenced by multiple factors, including genetic mutations that activate various oncogenic signaling pathways, including the TGF-&#946; pathway. Aberrant activation of TGF-&#946; signaling is correlated with tumor recurrence and metastasis. It has been shown that non-coding RNAs (ncRNAs) have crucial effects on cancer cell proliferation, migration, and metastasis. Upregulation of various ncRNAs, including long non-coding RNAs (lncRNA) and microRNAs (miRNAs), has been reported in several tumors, like cervical, ovarian, and endometrial cancers, but their cellular mechanisms remain to be investigated. Thus, recognizing the role of ncRNAs in regulating the TGF-&#946; pathway may provide novel strategies for better treatment of cancer patients. The present study summarizes recent findings on the role of ncRNAs in regulating the TGF-&#946; signaling involved in tumor progression and metastasis in gynecologic cancers.]]></description> </item><item><title><![CDATA[A Strategy based on Bioinformatics and Machine Learning Algorithms Reveals
Potential Mechanisms of Shelian Capsule against Hepatocellular Carcinoma]]></title><link>https://www.benthamscience.comarticle/137497</link><description><![CDATA[<p>Background: Hepatocellular carcinoma (HCC) is a prevalent and life-threatening form of cancer, with Shelian Capsule (SLC), a traditional Chinese medicine (TCM) formulation, being recommended for clinical treatment. However, the mechanisms underlying its efficacy remain elusive. This study sought to uncover the potential mechanisms of SLC in HCC treatment using bioinformatics methods. <p> Methods: Bioactive components of SLC were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), and HCC-related microarray chip data were sourced from the Gene Expression Omnibus (GEO) database. The selection criteria for components included OB ≧ 30% and DL ≧ 0.18. By integrating the results of differential expression analysis and weighted gene co-expression network analysis (WGCNA), disease-related genes were identified. Therapeutic targets were determined as shared items between candidate targets and disease genes. Protein-protein interaction (PPI) network analysis was conducted for concatenated genes, with core protein clusters identified using the MCODE plugin. Machine learning algorithms were applied to identify signature genes within therapeutic targets. Subsequently, immune cell infiltration analysis, single-cell RNA sequencing (sc-RNA seq) analysis, molecular docking, and ADME analysis were performed for the screened genes. <p> Results: A total of 153 SLC ingredients and 170 candidate targets were identified, along with 494 HCCrelated disease genes. Overlapping items between disease genes and drug candidates represented therapeutic genes, and PPI network analysis was conducted using concatenated genes. MCODE1 and MCODE2 cluster genes underwent Disease Ontology (DO), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Four signature genes (TOP2A, CYP1A2, CYP2B6, and IGFBP3) were identified from 28 therapeutic genes using 3 machine learning algorithms, with ROC curves plotted. Molecular docking validated the interaction modes and binding abilities between signature genes and corresponding compounds, with free binding energy all <-7 kcal/mol. Finally, ADME analysis revealed similarities between certain SLC components and the clinical drugs Sorafenib and Lenvatinib. <p> Conclusion: In summary, our study revealed that the mechanism underlying the anti-HCC effects of SLC involves interactions at three levels: components (quercetin, beta-sitosterol, kaempferol, baicalein, stigmasterol, and luteolin), pathways (PI3K-Akt signaling pathway, TNF signaling pathway, and IL-17 signaling pathway), and targets (TOP2A, CYP1A2, CYP2B6, and IGFBP3). This study provides preliminary insights into the potential pharmacological mechanisms of SLC in HCC treatment, aiming to support its clinical application and serve as a reference for future laboratory investigations.</p>]]></description> </item><item><title><![CDATA[miRNAs Delivery for Cancer-associated Fibroblasts’ Activation and Drug
Resistance in Cancer Microenvironment]]></title><link>https://www.benthamscience.comarticle/133978</link><description><![CDATA[Cancer-associated fibroblasts (CAFs) as a major component of cancer stroma contribute to diverse procedures of most solid tumors and might be a targeted cancer therapy approach. Their specified features, related signaling pathways, distinct biomarkers, and sub-populations need to be deciphered. There is a need for CAF extraction or induction for in vitro investigations. Some miRNAs could activate CAF-like phenotype and they also interfere in CAF-mediated drug resistance, aggressiveness, and metastatic behaviors of several cancer cell types. Due to the complex relevance of miRNA and CAFs, these non-coding oligonucleotides may serve as attractive scope for anti-cancer targeted therapies, but the lack of an efficient delivery system is still a major hurdle. Here, we have summarized the investigated information on CAF features, isolation, and induction procedures, and highlighted the miRNA-CAF communications, providing special insight into nano-delivery systems.]]></description> </item><item><title><![CDATA[The Voyage of Natural Chalcone: Isoliquiritigenin]]></title><link>https://www.benthamscience.comarticle/131884</link><description><![CDATA[This review aims to provide a comprehensive summary of the pharmacological effects of isoliquiritigenin, a natural chalcone. The data was gathered from a variety of research papers published till 2022. The extensive pharmacological features of ISL, including its anti-inflammatory, anti-influenza, anti-tyrosinase, anti-bacterial, anti-sarcoma, anti-oxidative, anti-leiomyoma, anticholera, anti-asthma, anti-diabetic, and anti-cancer activity, neuroprotective, hepatoprotective, and cardioprotective effects, may explain its practical applicability in the treatment and prevention of many illnesses. However, to confirm the target-organ toxicity or side effects, more research is required. The creation and design of new ISL analogues based on previously discovered techniques may benefit from this review.]]></description> </item><item><title><![CDATA[A Review on Graphene Analytical Sensors for Biomarker-based
Detection of Cancer]]></title><link>https://www.benthamscience.comarticle/134441</link><description><![CDATA[The engineering of nanoscale materials has broadened the scope of nanotechnology in a restricted functional system. Today, significant priority is given to immediate health diagnosis and monitoring tools for point-of-care testing and patient care. Graphene, as a one-atom carbon compound, has the potential to detect cancer biomarkers and its derivatives. The atom-wide graphene layer specialises in physicochemical characteristics, such as improved electrical and thermal conductivity, optical transparency, and increased chemical and mechanical strength, thus making it the best material for cancer biomarker detection. The outstanding mechanical, electrical, electrochemical, and optical properties of two-dimensional graphene can fulfil the scientific goal of any biosensor development, which is to develop a more compact and portable point-of-care device for quick and early cancer diagnosis. The bio-functionalisation of recognised biomarkers can be improved by oxygenated graphene layers and their composites. The significance of graphene that gleans its missing data for its high expertise to be evaluated, including the variety in surface modification and analytical reports. This review provides critical insights into graphene to inspire research that would address the current and remaining hurdles in cancer diagnosis.]]></description> </item><item><title><![CDATA[CD155-TIGIT Axis as a Therapeutic Target for Cancer
Immunotherapy]]></title><link>https://www.benthamscience.comarticle/130348</link><description><![CDATA[Immune checkpoint inhibitors (ICIs) have shown unprecedented efficacy in treating many advanced cancers. Although FDA-approved ICIs have shown promising efficacy in treating many advanced cancers, their application is greatly limited by the low response rate, immune-related adverse events (irAE), and drug resistance. Developing novel ICIs holds great promise to improve the survival and prognosis of advanced cancer patients. T-Cell immunoglobulin and ITIM domain (TIGIT) is an inhibitory receptor expressed on T cells, natural killer (NK) cells, and T regulatory cells. Increasing reports have shown that the disrupting CD155-TIGIT axis could activate the immune system and restore antitumor immune response. This review briefly summarized the role of TIGIT in tumor immune escape and targeting CD155-TIGIT axis drugs in preclinical and clinical trials for cancer immunotherapy.]]></description> </item><item><title><![CDATA[Mitochondrial Calcium Uniporter (MCU) that Modulates Mitochondrial
Calcium Uptake and Facilitates Endometrial Cancer Progression through
Interaction with VDAC1]]></title><link>https://www.benthamscience.comarticle/134439</link><description><![CDATA[<P> Background: Although endometrial cancer represents a frequently diagnosed malignancy of the female reproductive tract, we know very little about the factors that control endometrial cancer. <P> Objective: Our study was presented to investigate the function of MCU in endometrial tumorigenesis and the molecular mechanisms involved. <P> Materials and Methods: A total of 94 endometrial cancer patients were recruited into our cohort. MCU and VDAC1 expression was examined in tumor and normal tissues <i>via</i> immunohistochemistry and immunofluorescence. Associations of MCU and VDAC1 expression with clinicopathological characteristics were evaluated. After transfection with shRNA targeting MCU or full-length MCU plasmids, clone formation, wound healing, transwell and MitoTracker Red staining were separately presented in Ishikawa and RL95-2 cells. Moreover, Western blotting or immunofluorescence was utilized to examine the expression of MCU, VDAC1, Na<sup>+</sup>/Ca2<sup>+</sup>/Li<sup>+ </sup>exchanger (NCLX), and &#946;-catenin under VDAC1 knockdown and/or MCU overexpression or knockdown. <P> Results: MCU and VDAC1 expression were prominently up-regulated in endometrial cancer tissues and were significantly associated with histological grade, depth of myometrial invasion and lymph node status. MCU up-regulation enhanced clone formation, migration, and mitochondrial activity of endometrial cancer cells. The opposite results were investigated when MCU was silenced. MCU or VDAC1 silencing reduced the expression of MCU, VDAC1, NCLX, and β-catenin. Moreover, VDAC1 knockdown alleviated the promoting effect of MCU overexpression on the above proteins. <P> Conclusion: This investigation demonstrated that MCU-induced mitochondrial calcium uptake plays a critical role in endometrial tumorigenesis through interaction with VDAC1.</P>]]></description> </item><item><title><![CDATA[Advancement of Nanocarriers-based Therapeutics for Effective Management of
Colorectal Cancer]]></title><link>https://www.benthamscience.comarticle/132129</link><description><![CDATA[<p>Background: Colorectal cancer is still challenging for scientists and healthcare professionals. Conventional treatment methods are associated with various limitations in clinical bed and patient compliance. However, novel nanocarrier-based approaches have opened a new window for improved therapy and a new future perspective. <p> Introduction: Cancer is the deadliest disease globally and is challenging to healthcare systems. Colorectal cancer (CRC) is the third most common cancer in the world, affecting all age groups and is the most common cancer in 23 countries, as per the World Health Organization (WHO). <p> Methods: In this review, we addressed the nanocarrier-based strategic treatment of colorectal cancer, along with major findings, limitations, and future perspectives. For this, we thoroughly reviewed several literatures downloaded from prime sources, such as google scholar, Web of Science, PubMed, and Publon. To filter the exact data needed, we used keywords alone or in combination. Various relevant articles were obtained from the reference section of the selected papers. <p> Result and Discussion: It is necessary to have an effective and targeted treatment option to control CRC other than available remedies. Nanotechnology has been widely used to diagnose and treat several cancer types. Advances in nanomedicine and phytonanomedicine have promoted novel identification methods to treat colorectal cancer patients. There are several nanocarriers recommended for clinical purposes. However, to date, only a few clinically approved nanocarriers can load anticancer moieties and selectively bind to cancer cells. Some nanocarriers transport and release treatments to the target colorectal area but provide few benefits. <p> Conclusion: In this review, various nanoparticles (NPs) with unique properties have been discussed in relation to managing colorectal cancer, along with major outcomes of clinical trials and successful patents published so far.</p>]]></description> </item><item><title><![CDATA[Retracted: Advancement of Nanocarriers-based Therapeutics for Effective Management of
Colorectal Cancer]]></title><link>https://www.benthamscience.comarticle/129778</link><description><![CDATA[<p>The article titled “Advancement of Nanocarriers-based Therapeutics for Effective Management of Colorectal Cancer” was originally published in Current Indian Science, Volume 1, Issue 1, Pages 14, and was erroneously published twice in the same volume due to an administrative error. </p> <p> To maintain the integrity of the scholarly record, we have removed the duplicate publication and would like to retract it. This retraction is solely due to an inadvertent duplication on the part of the publisher, and the authors bear no responsibility for this mistake. Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused. </p> <p> We sincerely regret this error and apologize to the authors and readers for any confusion caused. We are implementing additional editorial checks to prevent such occurrences in the future. </p> <p> Bentham Science Disclaimer: </p> <p> It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure, or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication, the authors agree that the publishers have the legal right to take appropriate action against the authors if plagiarism or fabricated information is discovered. By submitting a manuscript, the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.</p>]]></description> </item><item><title><![CDATA[Melatonin as a Promising Agent for Cancer Treatment: Insights into
its Effects on the Wnt/beta-catenin Signaling Pathway]]></title><link>https://www.benthamscience.comarticle/130801</link><description><![CDATA[In recent years, substantial advances have been made in cancer treatment modalities. Yet, within the last three decades, neither cancer incidence nor the cancer-induced mortality rate has changed. Available anti-cancer chemotherapeutics possess remarkably restricted effectiveness and often have severe adverse effects. Hence, the identification of novel pharmaceutical agents that do not exhibit these major disadvantages is imperative. Melatonin, an important endogenous molecule synthesized and secreted by the pineal gland, is a promising chemical agent that has been comprehensively assessed over the last decades for its anti-inflammatory and anti-cancer properties. Melatonin is reportedly a significant inhibitor of cancer initiation, progression, and metastasis. The anti-- cancer potential of melatonin is principally mediated by reversing the up-regulated amounts of different transcription factors, growth factors, inflammatory cytokines, protein kinases, and other oncogenic agents. Also, melatonin often has signifcant inhibitory effects on cancer cell proliferation through either promoting apoptosis or inducing cell cycle arrest. The current review provides an insight into melatonin-induced effects against various human cancers with a particular focus on the regulation of Wnt/β-catenin signaling pathway.]]></description> </item><item><title><![CDATA[Deciphering Potential Role of Hippo Signaling Pathway in Breast Cancer: A
Comprehensive Review]]></title><link>https://www.benthamscience.comarticle/136774</link><description><![CDATA[Breast cancer is a heterogeneous disease and a leading malignancy around the world. It is a vital cause of untimely mortality among women. Drug resistance is the major challenge for effective cancer therapeutics. In contrast, cancer stem cells (CSCs) are one of the reasons for drug resistance, tumor progression, and metastasis. The small population of CSCs present in each tumor has the ability of self-renewal, differentiation, and tumorigenicity. CSCs are often identified and enriched using a variety of cell surface markers (CD44, CD24, CD133, ABCG2, CD49f, LGR5, SSEA-3, CD70) that exert their functions by different regulatory networks, i.e., Notch, Wnt/β-catenin, hedgehog (Hh), and Hippo signaling pathways. Particularly the Hippo signaling pathway is the emerging and very less explored cancer stem cell pathway. Here, in this review, the Hippo signaling molecules are elaborated with respect to their ability of stemness as epigenetic modulators and how these molecules can be targeted for better cancer treatment and to overcome drug resistance.]]></description> </item><item><title><![CDATA[Nanoparticles Containing Oxaliplatin and the Treatment of Colorectal Cancer]]></title><link>https://www.benthamscience.comarticle/136154</link><description><![CDATA[<P>Background: Colorectal cancer (CRC) is a highly widespread malignancy and ranks as the second most common cause of cancer-related mortality. <P> Objective: Cancer patients, including those with CRC, who undergo chemotherapy, are often treated with platinum- based anticancer drugs such as oxaliplatin (OXA). Nevertheless, the administration of OXA is associated with a range of gastrointestinal problems, neuropathy, and respiratory tract infections. Hence, it is necessary to devise a potential strategy that can effectively tackle these aforementioned challenges. The use of nanocarriers has shown great potential in cancer treatment due to their ability to minimize side effects, target drugs directly to cancer cells, and improve drug efficacy. Furthermore, numerous studies have been published regarding the therapeutic efficacy of nanoparticles in the management of colorectal cancer. <P> Methods: In this review, we present the most relevant nanostructures used for OXA encapsulation in recent years, such as solid lipid nanoparticles, liposomes, polysaccharides, proteins, silica nanoparticles, metal nanoparticles, and synthetic polymer-carriers. Additionally, the paper provides a summary of the disadvantages and limits associated with nanoparticles. <P> Results: The use of different carriers for the delivery of oxaliplatin increased the efficiency and reduced the side effects of the drug. It has been observed that the majority of research investigations have focused on liposomes and polysaccharides. <P> Conclusion: This potentially auspicious method has the potential to enhance results and enhance the quality of life for cancer patients undergoing chemotherapy. However, additional investigation is required to ascertain the most suitable medium for the transportation of oxaliplatin and to assess its efficacy through clinical trials.</P>]]></description> </item><item><title><![CDATA[Current use of Molecular Mechanisms and Signaling Pathways in Targeted Therapy of Prostate Cancer]]></title><link>https://www.benthamscience.comarticle/135720</link><description><![CDATA[Prostate cancer (PC) is identified as a heterogeneous disease. About 20 to 30% of PC patients experience cancer recurrence, characterized by an increase in the antigen termed serum prostate-specific antigen (PSA). Clinical recurrence of PC commonly occurs after five years. Metastatic castration-resistant prostate cancer (mCRPC) has an intricate genomic background. Therapies that target genomic changes in DNA repair signaling pathways have been progressively approved in the clinic. Innovative therapies like targeting signaling pathways, bone niche, immune checkpoint, and epigenetic marks have been gaining promising results for better management of PC cases with bone metastasis. This review article summarizes the recent consideration of the molecular mechanisms and signaling pathways involved in local and metastatic prostate cancer, highlighting the clinical insinuations of the novel understanding.]]></description> </item><item><title><![CDATA[To Investigate Growth Factor Receptor Targets and Generate Cancer
Targeting Inhibitors]]></title><link>https://www.benthamscience.comarticle/136165</link><description><![CDATA[Receptor tyrosine kinase (RTK) regulates multiple pathways, including Mitogenactivated protein kinases (MAPKs), PI3/AKT, JAK/STAT pathway, etc. which has a significant role in the progression and metastasis of tumor. As RTK activation regulates numerous essential bodily processes, including cell proliferation and division, RTK dysregulation has been identified in many types of cancers. Targeting RTK is a significant challenge in cancer due to the abnormal upregulation and downregulation of RTK receptors subfamily EGFR, FGFR, PDGFR, VEGFR, and HGFR in the progression of cancer, which is governed by multiple RTK receptor signalling pathways and impacts treatment response and disease progression. In this review, an extensive focus has been carried out on the normal and abnormal signalling pathways of EGFR, FGFR, PDGFR, VEGFR, and HGFR and their association with cancer initiation and progression. These are explored as potential therapeutic cancer targets and therefore, the inhibitors were evaluated alone and merged with additional therapies in clinical trials aimed at combating global cancer.]]></description> </item><item><title><![CDATA[Knockdown of PROM2 Enhances Paclitaxel Sensitivity in Endometrial Cancer Cells
by Regulating the AKT/FOXO1 Pathway]]></title><link>https://www.benthamscience.comarticle/134277</link><description><![CDATA[<P>Background: Endometrial cancer is a very common and highly lethal reproductive malignant tumour in women. Paclitaxel (PTX) is a usual drug utilized in chemotherapy for endometrial cancer. It has been uncovered that PROM2 participates in the progression of various cancers through playing a promoter. However, the regulatory function of PROM2 in PTX treatment for endometrial cancer remains unclear. </P><P> Methods: The cell viability (IC<sub>50</sub>) was examined through CCK8 assay. The mRNA and protein expressions of genes were measured through RT-qPCR and western blot. The proliferation was evaluated through colony formation and EdU assays. The cell apoptosis was assessed through flow cytometry. </P><P> Results: In this work, through bioinformatic analysis on online websites, it is found that the up-regulated expression of PROM2 existed in endometrial cancer. In addition, the survival probability of UCEC patients with high PROM2 expression was worse. This study adopted PTX treatment for obtaining the PTX-resistant cells (HEC-1A/PTX and KLE/PTX). Furthermore, suppression of PROM2 enhanced PTX sensitivity through decreasing IC<sub>50</sub> and proliferation in endometrial cancer. Additionally, knockdown of PROM2 facilitated cell apoptosis in HEC-1A/PTX and KLE/PTX cells. Next, we found that silencing of PROM2 retards the AKT/FOXO1 pathway. At last, rescue assays reversed the strengthened PTX sensitivity mediated by PROM2 inhibition after SC79 treatment (AKT activator). </P><P> Conclusion: Knockdown of PROM2 enhanced PTX sensitivity in endometrial cancer through modulating the AKT/FOXO1 pathway. This study hinted that PROM2 may be a useful therapeutic target for PTX treatment in endometrial cancer.</P>]]></description> </item><item><title><![CDATA[Bioactive Peptides: Potential Impact on the Treatment of Gastrointestinal
Cancers]]></title><link>https://www.benthamscience.comarticle/135550</link><description><![CDATA[We have reviewed the potential use of bioactive peptides in the treatment of gastrointestinal (GI) malignancies, which are a significant cause of morbidity and mortality globally. Conventional therapies, such as surgery, chemotherapy, and radiotherapy, are associated with numerous side effects that may lead to longterm complications. Bioactive peptides are short-chain amino acids that can be extracted from natural sources or synthesized, and they have various potential health benefits, including anti-inflammatory, anti-hypertensive, antioxidant, antimicrobial, and anti-cancer properties. Bioactive peptides can be acquired from animal or plant sources, and can be classified based on their function, such as ACE-inhibiting, antimicrobial, and electrolyte- regulating peptides. Recent studies have demonstrated the promising role of bioactive peptides in tumor suppression, especially when combined with conventional therapies. In this study, we have reviewed the beneficial properties of bioactive peptides and their role in suppressing tumor activity. The mechanisms of bioactive peptides in tumor suppression are discussed. We have further reviewed the findings of preclinical and clinical studies that have investigated the application of bioactive peptides in the treatment of GI cancers. This review highlights the potential use of bioactive peptides as a promising treatment method for GI malignancies to increase the quality of life of GI cancer patients.]]></description> </item><item><title><![CDATA[The Potential of Cannabidiol for Acute Respiratory Distress Syndrome in
COVID-19]]></title><link>https://www.benthamscience.comarticle/134721</link><description><![CDATA[COVID-19 disease manifests itself in a wide range of signs and symptoms, beginning with mild symptoms, such as fever, cough, and dyspnea, progressing to acute respiratory distress syndrome (ARDS) and death in some cases. The cytokine storm, or an excess of cytokines released locally, is assumed to be the primary cause of ARDS and mortality in COVID-19 patients. To enhance the survival rate of COVID-19 patients, early management of the cytokine storm with immunomodulators is crucial. Although the effectiveness of some immunosuppressants, such as corticosteroids and tocilizumab, has been studied in clinical trials, the administration of these drugs should be exercised cautiously. Cannabidiol (CBD) is a non-psychotropic phytocannabinoid from Cannabis sativa extracts with anti-inflammatory properties. This review is intended to discuss the possible utility of CBD for the management of COVID-19 patients, particularly those with ARDS.]]></description> </item><item><title><![CDATA[Recent Trends in Electrospun Antibacterial Nanofibers for Chronic Wound Management]]></title><link>https://www.benthamscience.comarticle/133762</link><description><![CDATA[Chronic wounds and lesions have a severe impact on the socioeconomic status and compliance of patients all over the world. Diabetes-related chronic, non-healing lesions may necessitate amputation of the damaged limb or organ. These skin lesions are susceptible to microorganisms that cause infections that impede the healing process. Despite the advances in medication development and sophisticated formulations, treating persistent wound infections remains difficult. Electrospun antimicrobial wound dressings offer considerable potential for lowering the risk of infection and accelerating the healing of chronic wounds. Electrospinning is a cost-effective, reproducible, simple, and multifaceted technique for encapsulating hydrophobic and hydrophilic therapeutic molecules within polymeric carriers with wide-ranging applications. In this review, we have discussed extensively the recent advances in electrospun nanofiber formulation techniques for use as wound dressings, as well as the entrapment of various antibacterial biomolecules, such as synthetic antibiotics, phytoconstituents, and metal nanoparticles, which have been embedded into the electrospun nanofibers, highlighting bioactive antibacterial agents capable of enhancing wound healing. In addition, we focus on the challenges currently being faced in the area of biomedicine as well as the opportunities for electrospinning-based nanomaterials.]]></description> </item><item><title><![CDATA[First Approval of Elacestrant as a Selective Estrogen Receptor
Degrader for the Treatment of Metastatic Breast Cancer]]></title><link>https://www.benthamscience.comarticle/131499</link><description><![CDATA[Elacestrant was approved by the US FDA on January 27, 2023, for treating postmenopausal women or adult men with estrogen receptor (ER)-positive, HER2- negative, ESR1-mutated advanced or metastatic breast cancer with disease progression prior to using at least one line of endocrine therapy. In this short perspective, physicochemical properties, dosage and administration, mechanism of action, pharmacodynamics, pharmacokinetics, drug interaction, and treatment-related adverse reactions of elacestrant are summarized.]]></description> </item><item><title><![CDATA[Statin as Repurposed Drug in Ovarian Cancer: A Comprehensive Review]]></title><link>https://www.benthamscience.comarticle/134499</link><description><![CDATA[With a prevalence rate of 6.6 per 100,000 women, ovarian cancer is the third most lethal gynecological tumor in the world. Several factors like family history, nulliparity, late menopause, genetic mutation, and an unhealthy lifestyle contribute to increasing the risk of ovarian cancer development. Novel research studies suggest that ovarian cancer may be caused by changes in the lipid metabolic profile that trigger inflammatory responses. Moreover, ovarian cancer patients will eventually experience chemoresistance. Statin, a competitive inhibitor of HMG-CoA reductase that is a lipid-lowering drug with pleiotropic effects, seems to be the best choice to deal with this therapeutic issue. The aim of this review is to highlight the pharmacotherapeutic potential of statins, especially the repurposing of statin drugs for antitumor mechanisms. This review will also provide a brief summary of the meta-analysis, and case-control observational studies carried out to examine the impact of statins on risk reduction and survival in ovarian cancer patients. Furthermore, this review will discuss the nanotechnological approach for improving the drug's bioavailability and safe and targeted delivery with controlled release of active ingredients, making statins more effective in preventing and treating ovarian cancer.]]></description> </item><item><title><![CDATA[Futibatinib: A Potent and Irreversible Inhibitor of Fibroblast Growth
Factor Receptors for Treatment of the Bile Duct Cancer]]></title><link>https://www.benthamscience.comarticle/130944</link><description><![CDATA[Cholangiocarcinoma is a rare type of cancer. Futibatinib is an irreversible, potent, selective inhibitor of fibroblast growth factor receptors (FGFR 1-4). On September 30, 2022, the US FDA first approved futibatinib to treat adult patients with bile duct cancer whose disease is unresectable, locally advanced, or metastatic intrahepatic cholangiocarcinoma harboring fibroblast growth factor receptor 2 (<i>FGFR2</i>) gene mutations or other classes of rearrangements. The approval of this medicine was based on phase 3 clinical trial results including an overall response rate (ORR) of 42% and a duration of response (DoR) of 9.7 months. This short perspective summarizes Futibatinib’s synthesis, physicochemical properties, dosage, route of administration, mechanism of action, binding mode, pharmacodynamics, pharmacokinetics, drug interactions, adverse events, and possible mechanism of resistance.]]></description> </item><item><title><![CDATA[Screening and Identification of Key Genes for Cervical Cancer, Ovarian
Cancer and Endometrial Cancer by Combinational Bioinformatic Analysis]]></title><link>https://www.benthamscience.comarticle/131295</link><description><![CDATA[<p>Introduction: Cervical cancer, ovarian cancer and endometrial cancer are the top three cancers in women. With the rapid development of gene chip and high-throughput sequencing technology, it has been widely used to study genomic functional omics data and identify markers for disease diagnosis and treatment. At the same time, more and more public databases containing genetic data have appeared. The result of the bioinformatic analysis can provide a diagnosis of new perspectives on cell origin and differences. <p> Methods: In this paper, three datasets about cervical cancer, ovarian cancer and endometrial cancer from GEO were used to dig out common DEGs (differentially expressed genes) among cervical cancer/ovarian cancer/endometrial cancer. DEGs contain 400 up-regulation genes and 157 down-regulation genes. <p> Results: The results of GO (gene ontology) functional enrichment analysis show that the BP (biological process) changes of DEGs are mainly in cell division, mitotic nuclear division, sister chromatid cohesion, and DNA replication. The CC (cell component) function enrichments of DEGs were mainly in the nucleoplasm, nucleus, condensed chromosome kinetochore, chromosome, centromeric region. The MF (molecular function) function enrichments of DEGs were mainly in protein binding. The results of the KEGG pathway analysis showed that the upregulation DEGs were mainly enriched in retinoblastoma gene in the cell cycle, cellular senescence, oocyte meiosis, and pathways in cancer, while the downregulation DEGs enriched in thiamine metabolism, protein processing in endoplasmic reticulum. Similarly, the function of the most significant module was enriched in cell division, condensed chromosome kinetochore, and microtubule motor activity. <p> Conclusion: In the result, 4 of the top 10 hub genes (CCNA2, CCNB1, CDC6 and CDK1) will provide help for future biomedical experimental research.</p>]]></description> </item><item><title><![CDATA[Alleviative Effects of Adipose Tissue-derived Stem Cells and &#945;-NETA on
Metabolic, Biochemical, and Endocrine Parameters in a Letrozole-induced Rat
Model of PCOS]]></title><link>https://www.benthamscience.comarticle/133672</link><description><![CDATA[<p>Background: Polycystic ovary syndrome (PCOS), the most prevalent reproductive disorder, is accompanied by hyperandrogenism (HA), ovulatory dysfunction (OD), and insulin resistance (IR). A number of reports indicate that adipokines play a vital role in the pathophysiology of PCOS. One of these adipokines is chemerin, which is engaged in metabolic disorders, especially obesity, diabetes, and PCOS. Based on the data, the circulating levels of chemerin and the expression of chemokine-like receptor-1 (CMKLR1) in white adipose tissue (WAT) of women with PCOS are significantly higher than in healthy ones. Currently, several scholars have emphasized the therapeutic capacities of stem cells, notably mesenchymal stem cells (MSCs), for the treatment of PCOS. <p> Objective: In this study, for the first time, the impacts of 2-(&#945;-naphthoyl) ethyltrimethylammonium iodide (&#945;- NETA), an antagonist of CMKLR1, adipose-derived stem cells (ADSCs), and their combinations on metabolic and endocrine aberrancies were assessed in the WAT and ovarian tissues of the letrozole (LET)-induced PCOS rats. <p> Methods: In the current study, 30 Wistar rats were randomly divided into five groups: control (n = 6), LET-induced PCOS (1.5 mg/kg p.o., n = 6), LET + ADSCs (10<sup>6</sup> ADSCs i.v., n = 6), LET + &#945;-NETA (10 mg/kg p.o., n = 6), and LET + ADSCs + &#945;-NETA (n = 6). The blood samples and adipose and ovarian tissues were obtained to evaluate the effects of ADSCs and &#945;-NETA on hormonal and metabolic parameters in the PCOS rats. <p> Results: Our findings showed that the administration of &#945;-NETA, ADSCs, and the combination of both favorably restored the irregular estrus cycle and considerably modulated the endocrine parameters in PCOS rats. In addition, these therapeutic factors remarkably regulated steroidogenic and adipogenic gene expressions, as well as the genes related to glucose metabolism and brown adipose tissue (BAT) markers in these animals. <p> Conclusion: These findings indicate that the combination of ADSCs and &#945;-NETA can successfully ameliorate metabolic and endocrine dysfunction in LET-induced PCOS rats, and this strategy could be a new therapeutic choice for patients with PCOS.</p>]]></description> </item><item><title><![CDATA[Novel Perspectives for the Diagnosis and Treatment of Gynecological
Cancers using Dysregulation of PIWI Protein and PiRNAs as
Biomarkers]]></title><link>https://www.benthamscience.comarticle/129496</link><description><![CDATA[The term “gynecological cancer” is used for a group of cancers occurring in the female reproductive system. Some of these cancers are ranked as the leading causes of death in developed and developing countries. The lack of proper diagnostic strategies is one of the most important reasons that make them lethal. PIWI-interacting RNAs or piRNAs are a class of small non-coding RNAs, which contain 24-32 nucleotides. These RNAs take part in some cellular mechanisms, and their role in diverse kinds of cancer is confirmed by accumulative evidence. In this review, we gather some information on the roles of these RNAs and members of the PIWI protein family to provide new insight into accurate diagnostic biomarkers and more effective anti-cancer drugs with fewer side effects.]]></description> </item><item><title><![CDATA[From Basics of Coordination Chemistry to Understanding Cisplatin-analogue Pt
Drugs]]></title><link>https://www.benthamscience.comarticle/133473</link><description><![CDATA[<p>Background: Cisplatin, a platinum complex discovered by Rosenberg in 1969, has long been known as the first metal-based anticancer agent. Since then, various similar derivatives of cisplatin have been investigated for pharmacological activity, and the approved complexes have been applied as drugs. <p> Objectives: The aims of the current study are: 1) to summarize the advantages and dose-limiting effects of the approved and unapproved chemotherapy platinum cytostatics, 2) to develop new strategies for the development of platinum anticancer drugs, and 3) to clarify the important factors for the mechanism of action of platinum complexes. <p> Methods: A search was conducted in the literature databases, and the obtained information was summarized and analyzed. <p> Results: Myelosuppression is the main dose-limiting effect and the reason for the disapproval of platinum complexes, such as picoplatin, enloplatin, miboplatin, sebriplatin, zeniplatin, spiroplatin, iproplatin, and ormaplatin. From the basic point of view of inorganic coordination chemistry, such as theoretical calculations, crystal structures of model complexes, docking structures with nucleic acid molecules, spectroscopy, and biological aspects, the importance of physicochemical properties of inorganic platinum complexes for their mechanism of action has been indicated. Spectroscopic methods, such as FTIR, NMR, X-ray crystal structure analysis, and fluorescence microscopy, are important for the investigation of the conformational changes in the binding of platinum complexes and DNA. <p> Conclusion: In the development of platinum complexes, strong anti-cancer drug activity, low toxicity, and resistance can be obtained by the application of polynuclear platinum agents, complexes with targeted activity, and nanoparticle formulations. Electronic structure, stereochemical, and thermodynamic properties are essential for understanding the reaction mechanism of platinum complexes.</p>]]></description> </item><item><title><![CDATA[GPR18 and GPR55-related Ligands Serving as Antagonists or Agonists:
Current Situation, Challenges and Perspectives]]></title><link>https://www.benthamscience.comarticle/130736</link><description><![CDATA[GPCR superfamily, the largest known family of membrane receptors, consists of six classes from A to F. GPR18 and GPR55, &#948;-branch of A class, had been reported to have no confirmed endogenous ligand and were named as “orphan receptors”. Previous studies suggest that both GPR18 and GPR55 are possibly related to the migration and proliferation of cancer cells, macrophages and other inflammation-associated immune cells. Thus, they may be potential targets for inflammation, cancer and analgesia therapy. In this paper, we aimed to summarize the chemical structures and bioactivities of the agonists and antagonists of GPR18 and GPR55; moreover, we have briefly discussed the challenges and future perspectives in this field. This review will be beneficial for further design and synthesis of efficient agonists and antagonists towards GPR18 and GPR55- related disease treatment.]]></description> </item><item><title><![CDATA[Endometrial Cancer Stem Cells Related Signaling Pathways]]></title><link>https://www.benthamscience.comarticle/130024</link><description><![CDATA[Endometrial cancer is gynecologic cancer that occurs in the uterus. Endometrial cancer stem cells (ECSC) are a small population of cancer cells that represent a crucial role in the metastasis of endometrial cancer cells to other organs in the body. ECSC can proliferate and give rise to mature cancer cells, which are found to participate in the aggressiveness of metastatic lesions. Therefore, targeting ECSC can be a valuable strategy for drug development against the metastasis of endometrial cancer. Previous studies have demonstrated that several signaling pathways, including Wnt, mTOR, EGFR, NOTCH, STAT3, VEGF, and SHH show modest effects and regulate the growth, epithelial-to-mesenchymal transition (EMT), and tumorigenesis of ECSC. Non-coding RNAs (ncRNAs) also play an important role in ECSC self-renewal, progression, and drug resistance. Hence, targeting these pathways might be a novel therapeutic approach for endometrial cancer diagnosis and therapy. This mini-review aims to characterize the main signaling pathways involved in the stimulation of ECSCs proliferation and tumorigenesis.]]></description> </item><item><title><![CDATA[Anti-obesity Properties of Phytochemicals: Highlighting their Molecular
Mechanisms against Obesity]]></title><link>https://www.benthamscience.comarticle/131872</link><description><![CDATA[Obesity is a complex, chronic and inflammatory disease that affects more than one-third of the world’s population, leading to a higher incidence of diabetes, dyslipidemia, metabolic syndrome, cardiovascular diseases, and some types of cancer. Several phytochemicals are used as flavoring and aromatic compounds, also exerting many benefits for public health. This study aims to summarize and scrutinize the beneficial effects of the most important phytochemicals against obesity. Systematic research of the current international literature was carried out in the most accurate scientific databases, e.g., Pubmed, Scopus, Web of Science and Google Scholar, using a set of critical and representative keywords, such as phytochemicals, obesity, metabolism, metabolic syndrome, etc. Several studies unraveled the potential positive effects of phytochemicals such as berberine, carvacrol, curcumin, quercetin, resveratrol, thymol, etc., against obesity and metabolic disorders. Mechanisms of action include inhibition of adipocyte differentiation, browning of the white adipose tissue, inhibition of enzymes such as lipase and amylase, suppression of inflammation, improvement of the gut microbiota, and downregulation of obesity-inducing genes. In conclusion, multiple bioactive compounds-phytochemicals exert many beneficial effects against obesity. Future molecular and clinical studies must be performed to unravel the multiple molecular mechanisms and anti-obesity activities of these naturally occurring bioactive compounds.]]></description> </item><item><title><![CDATA[The Comparison of Periostin Levels in Gingival Crevicular Fluid among
Patients with Endometrial Cancer and Chronic Periodontitis]]></title><link>https://www.benthamscience.comarticle/129795</link><description><![CDATA[<p>Background: Serum periostin in cancer patients and chronic periodontitis (CP) is the lowest and could be linked to the association between CP and endometrial cancer (EC). Periostin is a matricellular protein secreted by fibroblasts associated with cancer and is also secreted in chronic inflammatory conditions such as CP. <p> Objective: The aim of this study is to compare the GCF periostin level among CP, EC, and healthy people and the evaluation of the plausible role of periostin in this association. <p> Methods: This case-control study was conducted on 80 participants including 20 people with both EC and CP (EC-CP), 20 only CP cases (H-CP), 20 only EC cases (EC-H), and 20 healthy people (H-H). Then, the gingival crevicular fluid (GCF) periostin levels for all the participants were measured through enzyme-linked immunosorbent assay (ELISA). Finally, the data were analyzed using Stata software version 11. <p> Results: The mean value of periostin levels was significantly different between groups (p < 0.001) and the lowest and highest mean was observed in EC-CP and H-H groups, respectively. The mean of GCF periostin before treatment in the EC-CP group was 2.14 which was lower than that after treatment; however, this difference was not significant (p = 0.086). Also, the mean of GCF periostin in the H-CP group was 3.96 before non-surgical treatment and after treatment it significantly raised to 6.79 (p = 0.049). <p> Conclusion: Periostin is a potential biomarker for CP diagnosis in EC patients and also can be used to prevent CP. However, further studies are required to confirm this role.</p>]]></description> </item><item><title><![CDATA[Caveolae’s Behavior in Norm and Pathology]]></title><link>https://www.benthamscience.comarticle/131585</link><description><![CDATA[<p>Objectives: Caveolins are universal multifunctional physiologically active microparticles that collaborate in the caveolae formation to maintain the metabolic homeostatic balance of the cells. In fact, remarkable advances in the molecular biopathology of caveolae have been made in recent years by exploring the role of caveolae in norm and physiopathology. <p> Methods: The current literature data on the caveolae behavior in norm and pathology were revised. <p> Results: Caveolae are expressed in various cell types, highly concentrated in endothelial cells, cardiomyocytes, and epithelial cells. Physiologically, caveolae contribute to maintaining a signaling balance between the various homeostatic processes, including pro-growth and pro-survival, such as endothelial nitric oxide synthase, glycogen synthase kinase-3&#946;, p42/p44 mitogen-activated protein kinase, PKA, SFK, PKC, Akt through regulation of tyrosine kinases, G protein-coupled receptor, endothelial nitric oxide synthase, and MAPK pathways, and their signaling dysfunction is directly attributed to the pathogenesis of cardiovascular diseases, regeneration inhibition, neurodegenerative diseases, infection, osteoporosis, diabetes, and tumour induction and progression. <p> Conclusion: Regulation of the ratio and penetrance of caveolae activity/expression is a clinically significant potential therapeutic strategy to enhance the current therapies and eliminate the etiopathogenetic pathway of rising homeostatic disorders.</p>]]></description> </item><item><title><![CDATA[Diagnostic and Management Challenges of Rapid Lung Metastasis of
Gestational Trophoblastic Neoplasia after a Non-molar Pregnancy: A Case
Report]]></title><link>https://www.benthamscience.comarticle/130061</link><description><![CDATA[<P>:Background: Pulmonary metastasis of pregnancy-related rare gestational trophoblastic disease is common, and a patient’s rapid clinical deterioration leads to a poor prognosis. <P> Case Presentation: We report a case of a non-pregnant woman with severe respiratory symptoms masquerading as pulmonary infection who was diagnosed with pulmonary metastasis of the gestational trophoblastic disease. <P> Conclusion: The timely diagnosis of pulmonary metastasis was the key aspect in the management of our case, and she survived and was discharged to home after a long hospitalization course.</P>]]></description> </item><item><title><![CDATA[Repurposing some of the Well-known Non-steroid Anti-inflammatory
Drugs (NSAIDs) for Cancer Treatment]]></title><link>https://www.benthamscience.comarticle/129166</link><description><![CDATA[Drug repurposing is a strategy used to develop new treatments based on approved or investigational drugs outside the scope of their original clinical indication. Since this approach benefits from the original toxicity data of the repurposed drugs, the drug-repurposing strategy is timesaving, and inexpensive. It has a higher success rate compared to traditional drug discovery. Several repurposing candidates have been identified in silico screening and in vitro methodologies. One of the best examples is non-steroidal anti-inflammatory drugs (NSAIDs). Tumor-promoting inflammation is one of the hallmarks of cancer, revealing a connection between inflammatory processes and tumor progression and development. This explains why using NSAIDs in the context of neoplasia has become a topic of interest. Indeed, identifying NSAIDs with antitumor activity has become a promising strategy for finding novel cancer treatment opportunities. Indeed, several commercial anti-inflammatory drugs, including aspirin, ibuprofen, diclofenac, celecoxib, tepoxalin and cyclovalone, naproxen, and indomethacin have presented antitumor activity, and some of them are already in clinical trials for cancer treatment. However, the benefits and complications of using NSAIDs for cancer treatment must be carefully evaluated, particularly for cancer patients with no further therapeutic options available. This review article provides insight into the drug repurposing strategy and describes some of the well-known NSAIDs that have been investigated as repurposed drugs with potential anticancer activity.]]></description> </item><item><title><![CDATA[Aberrant Lipid Metabolism in Cancer: Current Status and Emerging
Therapeutic Perspectives]]></title><link>https://www.benthamscience.comarticle/131962</link><description><![CDATA[<p>It is now an undisputed fact that cancer cells undergo metabolic reprogramming to support their malignant phenotype, and it is one of the crucial hallmarks which enables cancer cells to facilitate their survival under variable conditions ranging from lack of nutrients to conditions, such as hypoxia. Recent developments in technologies, such as lipidomics and machine learning, have underlined the critical effects of altered lipid metabolism in tumorigenesis. The cancer cells show elevated de novo fatty acid synthesis, an increased capacity to scavenge lipids from their environment, and enhanced fatty acid oxidation to fulfill their need for uncontrolled cellular proliferation, immune evasion, tumor formation, angiogenesis, metastasis, and invasion. Besides, important genes/ proteins involved in lipid metabolism have been proposed as prognostic indicators in a variety of cancer types linked to tumor survival and/or recurrence. Consequently, several approaches are being explored to regulate this metabolic dysregulation to subvert its tumorigenic properties in different types of cancers. The present review details the significance of lipid metabolism in cancer progression, the critical enzymes involved therein, and their regulation. <p> Moreover, the current findings of the interplay between the oncogenic pathways and the lipid metabolic enzymes are elucidated briefly. The therapeutic implications of modulating these aberrations for the advancement of anti-cancer therapies are also discussed. Although the understanding of altered lipid metabolism in cancer initiation and progression is still in its infancy and somewhat obscure, its in-depth comprehension will open promising therapeutic opportunities for the development of novel and promising strategies for cancer treatment and management.</p>]]></description> </item><item><title><![CDATA[Significance of Beta-Blocker in Patients with Hypertensive Left Ventricular
Hypertrophy and Myocardial Ischemia]]></title><link>https://www.benthamscience.comarticle/129214</link><description><![CDATA[<p> Background: Arterial Hypertension (HTN) is a key risk factor for left ventricular hypertrophy (LVH) and a cause of ischemic heart disease (IHD). The association between myocardial ischemia and HTN LVH is strong because myocardial ischemia can occur in HTN LVH even in the absence of significant stenoses of epicardial coronary arteries. </p><p> Objective: To analyze pathophysiological characteristics/co-morbidities precipitating myocardial ischemia in patients with HTN LVH and provide a rationale for recommending beta-blockers (BBs) to prevent/treat ischemia in LVH. </p><p> Methods: We searched PubMed, SCOPUS, PubMed, Elsevier, Springer Verlag, and Google Scholar for review articles and guidelines on hypertension from 01/01/2000 until 01/05/2022. The search was limited to publications written in English. </p><p> Results: HTN LVH worsens ischemia in coronary artery disease (CAD) patients. Even without obstructive CAD, several pathophysiological mechanisms in HTN LVH can lead to myocardial ischemia. In the same guidelines that recommend BBs for patients with HTN and CAD, we could not find a single recommendation for BBs in patients with HTN LVH but without proven CAD. There are several reasons for the proposal of using some BBs to control ischemia in patients with HTN and LVH (even in the absence of obstructive CAD). </p><p> Conclusion: Some BBs ought to be considered to prevent/treat ischemia in patients with HTN LVH (even in the absence of obstructive CAD). Furthermore, LVH and ischemic events are important causes of ventricular tachycardia, ventricular fibrillation, and sudden cardiac death; these events are another reason for recommending certain BBs for HTN LVH.</p>]]></description> </item><item><title><![CDATA[The Protective Effects of Silymarin on the Reproductive Toxicity: A
Comprehensive Review]]></title><link>https://www.benthamscience.comarticle/129155</link><description><![CDATA[The reproductive system is extremely vulnerable to chemotherapy drugs, ionizing radiation, toxic heavy metals, chemicals, and so on. These harmful stimuli are able to induce oxidative damage, apoptosis, inflammation, and other mechanisms in the reproductive organs, leading to different adverse reproductive effects. It was shown that using medicinal plants (medicinal herbs) can be an effective medication for the prevention and treatment of multiple health conditions. Silymarin is a medicinal herb extract, obtained from the seeds of Silybum marianum. This herbal agent is a nontoxic agent even at relatively high physiological dose values, which suggests that it is safe for use in the treatment of different diseases. The hepato-, neuro-, cardio- and nephro-protective effects of silymarin have been assessed previously. The protective activities of silymarin can point to anti-oxidant, anti-apoptotic, anti-inflammatory, anti-fibrotic, immunomodulatory, and membrane-stabilizing properties. In this review, we aim to summarize current studies on the protective potentials of silymarin against reproductive toxicity. The molecular mechanisms of silymarin protection against cellular toxicity are also studied. Moreover, the findings obtained from improved formulations and delivery systems of silymarin have been addressed.]]></description> </item><item><title><![CDATA[LSINCT5: A Novel lncRNA in Cancers]]></title><link>https://www.benthamscience.comarticle/129027</link><description><![CDATA[<p> Background: Long chain non-coding RNAs (lncRNA) are a kind of transcript that is around 200 nucleotides long and can engage in life activities <i>via</i> epigenetic, transcriptional, and post-transcriptional regulation. One of the key members of lncRNAs, long stress-induced noncoding transcripts 5 (LSINCT5), is localized at Chr 5p and has been reported to be abnormally expressed in a range of cancers. We present a comprehensive review of LSINCT5&#039;s aberrant expression and regulatory mechanisms in malignant tumors. </p><p> Methods: The included studies were retrieved and summarized through the PubMed database using the keywords “LSINCT5” and “Cancer” in detail. </p><p> Results: LSINCT5 behaves as an oncogene and abundantly expresses in malignant tumorigenesis and progression. By sponging microRNAs (miRNA), interacting with proteins, participating in cellular transduction, and being regulated by transcription factors, LSINCT5 can stimulate malignant behavior in a variety of tumor cells, including proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Furthermore, dysregulated LSINCT5 is usually associated with a poor prognosis. </p><p> Conclusion: LSINCT5 has the potential to become a tumor diagnostic and prognostic marker, generating new access to clinical applications.</p>]]></description> </item></channel></rss>