Methods: We executed Mendelian randomization (MR) analysis to establish causal connections between these conditions and seven distinct categories of DTCs, including colorectal carcinoma (CRC), hepatocellular cancer (HCC), esophageal malignancy (ESCA), pancreatic adenocarcinoma (PAAD), biliary tract carcinoma (BTCs), gastric carcinoma (GC), and small intestine neoplasm (SIC). Leveraging instrumental variables (IVs) obtained from GWAS data of the FinnGen database, we employed a range of analytical methodologies, including inverse-variance weighting multiplicative random effects (IVW_MRE), inverse-variance weighting fixed effects (IVW_FE), maximum likelihood (ML), weighted median (WM), MR‒Egger regression, and the MR-PRESSO test.

Results: We observed a substantial linkage between genetically predicted constipation and increased vulnerability to PAAD (OR = 2.29, 95% CI: 1.422-3.69, P = 0.001) via the IVW method. Following the removal of outlier SNPs through MR-PRESSO, genetically predicted IBS was affiliated with an increased risk of CRC (OR = 1.17, 95% CI: 1-1.37, P = 0.05). Nonetheless, decisive causal correlations of constipation or IBS with other DTCs remain elusive.

Conclusion: In summary, genetically predicted constipation was associated with an augmented PAAD risk, and IBS was associated with an increased CRC susceptibility within European cohorts, in agreement with some observational studies. Nevertheless, the causal associations of constipation and IBS with other DTCs remain inconclusive.

Objective: The aim of this review was to discuss several important deregulated miRNAs that are involved in the p53 signaling pathway in BC, especially the TNBC subtype. Finally, miRNAs’ involvement in tumor properties and their applications as diagnostic, prognostic, and therapeutic agents have been elaborated in detail.

Results: The miRNA expression profile of BC is involved in tumor-grade estrogen receptor (ER) and progesterone receptor (PR) expression, and other pathological properties from luminal A to TNBC/basal-like subtypes via p53 signaling pathways.

Conclusion: Developing our knowledge about miRNA expression profile in BC, as well as molecular mechanisms of initiation and progression of BC can help to find new prognostic, diagnostic, and therapeutic biomarkers, which can lead to a suitable treatment for BC patients.

Antineoplastic medications that cause oxidative stress by raising ROS and blocking antioxidant mechanisms have recently attracted much interest. The rapid accumulation of ROS impairs redox balance and damages cancer cells severely. Here, we discuss ROS-instigating malignancy therapy and the antineoplastic mechanism used by prooxidative drugs.

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.

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.

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.

Methods: A total of 19 patients who underwent preoperative spectral CT dual-phase enhancement and who were diagnosed with HCC by postoperative pathology were prospectively selected. Patients with ≥10% Ki67-positive tumor cells formed a high-Ki67 group, and those with <10% Ki67- positive cells formed a low-Ki67 group. The iodine concentrations (ICs) of the lesion and the descending aorta were measured during the arterial and venous phases. Relative iodine concentration (RIC) was calculated thus: RIC=IC_lesion/IC_{descending aorta}. CT values of the lesions at 40 and 70 keV were measured during the enhanced arterial and venous phases. The slope of the spectral curve (λ) was calculated thus: λ = (40 keV-70 keV) /(70-30). To compare the differences in quantitative parameters between the high- and low-Ki67 groups, either an independent samples t-test (normal distribution) or a Mann–Whitney U test (non-normal distribution) was used. Receiver operating characteristic curves were used to evaluate the effectiveness of spectral CT parameters in distinguishing between high-Ki67 and low-Ki67 groups. Pearson correlation analysis was used to evaluate the correlation between spectral CT quantitative parameters and Ki67 expression.

Results: IC, RIC and λ values for the high-Ki67 group in arterial and venous phases were higher than those for the low-Ki67 group, P < 0.05. IC, RIC, and λ values in the arterial phase were 0.83, 0.89, and 0.75, respectively; in the venous phase, the values of these three parameters were 0.76, 0.77, and 0.69, respectively. IC, RIC, and λ were positively correlated with Ki67 expression in both arterial and venous phases, with a highest correlation of 0.82 for arterial-phase RIC.

Conclusion: The quantitative parameters of spectral CT in HCC were correlated with Ki67 expression. This finding may make it easier for clinicians to determine whether a tumor is high or low in Ki67 before surgery.

Objective: The study aimed to introduce the application of Raman spectroscopy to tumor detection. We have introduced the current mainstream Raman spectroscopy technology and related application research.

Methods: This article has first introduced the grim situation of malignant tumors in the world. The advantages of tumor diagnosis based on Raman spectroscopy have also been analyzed. Secondly, various Raman spectroscopy techniques applied in the medical field are introduced. Several studies on the application of Raman spectroscopy to tumors in different parts of the human body are discussed. Then the advantages of combining deep learning with Raman spectroscopy in the diagnosis of tumors are discussed. Finally, the related problems of tumor diagnosis methods based on Raman spectroscopy are pointed out. This may provide useful clues for future work.

Conclusion: Raman spectroscopy can be an effective method for diagnosing tumors. Moreover, Raman spectroscopy diagnosis combined with deep learning can provide more convenient and accurate detection results.

Case presentation: We presented a case of a 72-year-old female who was admitted to our hospital for chest pain and hematemesis within several minutes after chewing betel nut. Gastroscopy showed two longitudinal ridge-like mucosal eminences in the esophagus located 20 cm from the incisors down to the gastric cardia, which was similar to varices. At last, a CT scan showed concentric-circle thickening of the esophagus wall, suggesting hematomas. Our treatment included fasting, inhibiting gastric acid and maintaining blood volume. After one week of medical treatment, rechecked gastroscopy showed that esophageal hematomas were gradually absorbed, with the formation of multiple shallow ulcers.

Conclusion: The acute toxicity of chewing betel nut can be easily overlooked. Patients who experience chest pain or hematemesis after chewing betel nut products,especially those who take aspirin at the same time, need to be alert to esophageal hematoma.

Background: The presence of iodine in iodinated contrast agents (ICAs) can impede the effectiveness of radioactive iodine treatment (RAIT) and diagnostic scans in individuals diagnosed with DTC, as it can engage in competitive interactions with 131I. According to established guidelines, it is recommended to postpone RAIT for a period of three to four months in individuals who have had prior exposure to ICAS. The measurement of spot urine iodine concentration is a valuable indicator for assessing the overall iodine content throughout the body.

Objective: The objective is to identify the optimal timing for administering postoperative RAIT in DTC patients.

Methods: At various time points after surgery, a cohort of 467 random urine samples (126 male samples, 341 female samples, age (45±12 years)) was obtained from 269 DTC patients. The samples were analyzed for urinary iodine and urinary creatinine levels, and the urinary iodine/urine creatinine ratio (I/Cr) was computed. All samples were divided into two groups according to whether eCT before operation: the non-enhanced CT (eCT-) group and the enhanced CT (eCT+) group. The urine samples in the eCT- group were categorized into four subgroups according to the duration of strict low iodine diet (LID): (eCT-I+) no LID; (eCT-I-2W) 2 weeks of LID; (eCT-I-4W) 4 weeks of LID; and (eCT-I-6W) 6 weeks of LID. The last three groups were merged into the eCT- and effective LID group (eCT- I-). The urine samples from the eCT+ group were categorized into five subgroups: (0.5M eCT+)0.5 month after eCT+; (1M eCT+)1 month after eCT+; (2M eCT+) 2 months after eCT+; (3M eCT+) 3 months after eCT+; (≥4M eCT+) ≥4 months after eCT+. In addition, the patients within 2 months after eCT+ were divided into 2 groups according to their LID: no effective LID group (eCT+ I+) and effective LID group (eCT+ I-). Utilizing the Kruskal-Wallis and Mann-Whitney U rank sum tests, the differences in I/Cr between groups were compared.

Results: In the eCT-group, the I/Cr ratios of eCT-I-2W, eCT-I-4W, and eCT-I-6W were significantly lower than those of eCT-I+ (χ2 values: 4.607.99, all P 0.05). However, there was no significant difference in I/Cr between eCT-I-2W, eCT- I-4W, and eCT-I-6W (2 values: 0.591.31, all P > 0.05). Significantly higher I/Cr values were observed in 0.5M eCT+ and 1M eCT+ than in eCT-I+ (χ2 values: 3.22 and 2.18, respectively, all P<0.05). There was no significant difference in I/Cr between 2M eCT+ and eCT-I+ (χ2 = 0.76, P = 0.447). The I/Cr rations of 3M eCT+, ≥4M eCT+ were not significantly different with eCT-I- (χ2 values: 1.76; 0.58; all P > 0.05). However, they were considerably lower than eCT-I+ (χ2 values: 7.03; 5.22; all P<0.05). The I/Cr for patients who underwent eCT within two months (eCT+ I-, eCT+ I+) did not differ significantly (χ2 = 1.79, P = 0.073).

Conclusion: For patients who are considering receiving radioactive iodine therapy (RAIT) following a diagnosis of differentiated thyroid cancer (DTC), it is recommended that the interval between RAIT treatment and enhanced computed tomography [eCT] scans be conducted at least three months.

Case Presentation: The patient underwent gastric endoscopy revealing an extensive lower esophageal varix protruding into the proximal stomach, subsequently treated with banding. The stomach and duodenum were found to contain fresh blood and blood clots indicating acute bleeding.

An urgent CT scan identified active bleeding (extravasation) at segment V and blood accumulation at the confluence of the right and left biliary drains. This was followed by celiac and selective hepatic digital subtraction angiography (DSA).

Conclusion: This case study outlines the occurrence of a hepatic artery pseudoaneurysm six months after percutaneous insertion of bilateral biliary drains. The pseudoaneurysm manifested precisely at the confluence of the right and left drains. The reported delayed complication may have resulted from friction between the drains at the confluence or erosion of the adjacent artery by the drains. The insights gained from this case shed light on the causes and preventive measures for potential delayed complications associated with percutaneous biliary drain placement.

Case Report: A 54-year-old patient underwent surgery twice to remove primitive and recurrent cardiac sarcomas of the left atrium. The appearance of a further relapse required radiotherapy as the only possible treatment. Cardiac MRI was then performed to define the degree of atrial mass invasiveness, and 18F-FDG PET/CT was performed to assess the activity and staging of the cardiac lesion. It revealed high 18F-FDG uptake not only in the left atrium lesion but also in a pancreatic lesion with elevated 18F-FDG uptake (SUV max 5.5). The pancreatic biopsy performed a few days later confirmed the myxoid sarcoma metastasis, and surgeons defined it as not operable due to the patient’s clinical condition. Radiotherapy was then urgently performed with the VMAT technique. After 40 days, a cardiac MRI showed a reduction in the cardiac mass with improvement in the respiratory and cardiac symptoms; then, the patient started chemotherapy. One year after diagnosis, the patient is still alive and is receiving chemotherapy with gemcitabine and docetaxel with good compliance.

Conclusion: The correct and timely management of a patient suffering from a rare oncological disease has allowed a better and longer survival, especially due to VMAT, a sophisticated procedure that requires high expertise. This case also demonstrates that cardiac MRI and whole-body imaging procedures, such as 18FDG PET/CT, can be useful in staging patients with oncological diseases.

Methods: A retrospective analysis was conducted on a patient with synchronous CRC and ccRCC who underwent ¹⁸F-FDG PET/CT and contrast-enhanced CT before treatment. Databases were analyzed to identify differentially expressed genes between CRC and ccRCC, and co-expression genes were extracted for RCC and CRC.

Results: ¹⁸F-FDG PET/CT revealed intense metabolic activity in the primary colorectal lesion (SUVmax 13.2), while a left renal mass (diameter = 35 mm) was observed with no significant uptake. Contrast-enhanced CT during the arterial phase showed heterogeneous intense enhancement of the renal lesion, and the lesion washed out earlier than in the renal cortex in the nephrographic and excretory phases, indicating ccRCC. The histopathological results confirmed synchronous double primary malignant tumors. Our bioinformatic analysis results showed that synchronous occurrence of CRC and ccRCC may correlate with simultaneous expression of Carbonic Anhydrase 9 (CA9), integrin-binding sialoprotein (IBSP), and Fibrinogen γ chain (FGG).

Conclusion: ¹⁸F-FDG PET/CT combined with contrast-enhanced CT is an effective diagnostic tool in evaluating synchronous CRC and RCC. By analyzing this clinical case and conducting bioinformatic analysis, we improved our current understanding of the mechanisms underlying synchronous tumors.

Methods: For the identification of GI illnesses, such as polyps, stomach ulcers, and bleeding, endoscopy is the gold standard in the medical imaging industry. The numerous images produced by endoscopy require an enormous amount of time for the specialist to diagnose the disease. It makes manual diagnosis difficult and has sparked research on automatic computer-based approaches to diagnose all the generated images quickly and accurately. AI-based algorithms have already been used in endoscopy images with promising outcomes and have enhanced disease identification and classification with precision. However, there are still a lot of issues to be solved, including figuring out potential biases in algorithms and improving interpretability and generalizability.

Results: The proposed GastroNet model creates a system for classifying digestive problems for the Kvasir Version 1 dataset. The framework consists of different CNN layers with multiple filters, and average max-pooling is used to extract image features. The optimization of network parameters is done using the Stochastic Gradient Descent (SGD) algorithm.

Conclusion: Finally, the robustness of the proposed model is compared with other state-of-the-art models like VGG 19, ResNet 50, Inception, and Xception in terms of evaluation metrics.

Objective: To investigate the clinical efficacy of EBUS-TBNA in the diagnosis and differential diagnosis of mediastinal and hilar lesions.

Methods: A retrospective observational study was undertaken to investigate patients diagnosed with mediastinal and hilar lymphadenopathy based on imaging at our hospital from 2020 to 2021. After evaluation, EBUS TBNA was used and data including the puncture site, postoperative pathology, and complications were recorded.

Results: Data from 137 patients were included in the study, of which 135 underwent successful EBUS TBNA. A total of 149 lymph node punctures were performed, of which 90 punctures identified malignant lesions. The most common malignancies were small-cell lung carcinoma, adenocarcinoma, and squamous cell carcinoma. Forty-one benign lesions were identified, resulting from sarcoidosis, tuberculosis, and reactive lymphadenitis, amongst others. Follow-up findings showed that 4 cases were malignant tumors, with 1 case of pulmonary tuberculosis and 1 case of sarcoidosis). Four specimens where lymph node puncture was insufficient were subsequently confirmed by other means. The sensitivity of EBUS TBNA for malignant lesions, tuberculosis and sarcoidosis in mediastinal and hilar lesions was 94.7%, 71.4%, and 93.3%, respectively. Similarly, the negative predictive values (NPV) were 88.9%, 98.5%, and 99.2%, and the accuracy was 96.3%, 98.5%, and 99.3%.

Conclusion: EBUS TBNA is an effective and feasible approach for the diagnosis of mediastinal and hilar lesions that is minimally invasive and safe.

Methods: An initial assessment was executed using a NEMA phantom to compare image quality engendered by OSEM and HYPER Iterative algorithms. Parameters such as BV, COV, and CRC were meticulously evaluated. Subsequently, a prospective cohort study was conducted on 50 patients, employing both reconstruction algorithms. The study was compartmentalized into distinct acquisition time and dosage groups. Lesions were further categorized into three size-based groups. Quantifiable metrics including SD of noise, SUV_max, SNR, and TBR were computed. Additionally, the differences in values, namely ΔSUV_max, ΔTBR, %ΔSUV_max, %ΔSD, and %ΔSNR, between OSEM and HYPER Iterative algorithms were also calculated.

Results: The HYPER Iterative algorithm showed reduced BV and COV compared to OSEM in the phantom study, with constant acquisition time. In the clinical study, lesion SUV_max, TBR, and SNR were significantly elevated in images reconstructed using the HYPER Iterative algorithm in comparison to those generated by OSEM (p < 0.001). Furthermore, an amplified increase in SUV_max was predominantly discernible in lesions with dimensions less than 10 mm. Metrics such as %ΔSNR and %ΔSD in HYPER Iterative exhibited improvements correlating with reduced acquisition times and dosages, wherein a more pronounced degree of enhancement was observable in both ΔSUV_max and ΔTBR.

Conclusion: The HYPER Iterative algorithm significantly improves SUV_max and reduces noise level, with particular efficacy in lesions measuring ≤ 10 mm and under conditions of abbreviated acquisition times and lower dosages.

Methods: A retrospective observational study was conducted on all children with a haemato-oncology diagnosis or who underwent haematopoietic stem cell transplantation (HSCT) and who were admitted to the Hong Kong Children’s Hospital PICU over a one-year period. Infection characteristics and patient outcomes were evaluated and compared between different sub-groups. Univariable and multi-variable analyses were employed to identify risk factors associated with the development of active infection.

Results: Forty-five (36.3%) of 124 critically ill haemato-oncology admissions to PICU were associated with infections, of which 31 (25%) admissions involved bacterial infections, 26 (20.9%) involved viral infections and 6 (4.8%) involved fungal infections. Bloodstream infection was the most common type of infection. More than half (61.3%) of the bacterial infections were due to an antibiotic-resistant strain. After adjusting for confounding variables, post-HSCT status and neutropenia were significantly associated with active infections.

Conclusion: Infections in critically-ill haemato-oncological patients are associated with post haematopoietic stem cell transplant status and neutropenia. Further study is warranted to review effective strategies that may mitigate the likelihood of infection in this patient population.

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.

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 < 0.001; HR = 3.97; 95% CI, 1.80-8.73; p < 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 < 0.001), and smoking history (OR = 0.27; 95% CI, 0.15-0.49; p < 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).

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.

Methods: A Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect lncRNA NUTM2A-AS1 expression in CRC cell lines. Cell counting kit 8 (CCK-8) assay and flow cytometry were used to examine the biological functions of lncRNA NUTM2A-AS1 in the proliferation and apoptosis of CRC cells. RT-qPCR and western blot were implemented for the detection of cell proliferation-, apoptosis-related proteins, and FAM3C. Bioinformatics analysis and dual- luciferase reporter assays were utilized to identify the mutual regulatory mechanism of ceRNAs.

Results: lncRNA NUTM2A-AS1 notably elevated in CRC cell lines and the silenced of NUTM2A- AS1 declined proliferation and facilitated apoptosis. Mechanistically, NUTM2A-AS1 was transcriptionally activated by histone H3 on lysine 27 acetylation (H3K27ac) enriched at its promoter region, and NUTM2A-AS1 acted as a sponge for miR-126-5p, leading to the upregulation of FAM3C expression in CRC cell lines.

Conclusion: Our research proposed NUTM2A-AS1 as an oncogenic lncRNA that facilitates CRC malignancy by upregulating FAM3C expression, which might provide new insight and a promising therapeutic target for the diagnosis and treatment of CRC.

Method: 34 patients in the drug group received 4 capsules of Mastic pill plus Omeprazole capsule 20 mg daily. 34 patients in the placebo group received the same dosing of Omeprazole and placebo. The medication was given to patients for a total duration of 4 weeks. All patients were requested to fill out the modified GERD-HRQL questionnaire at the beginning and every two weeks for a total duration of six weeks.

Result: Reflux, and heartburn severity score as well as disruption of personal life score significantly reduced in both groups, but it was more remarkable in the drug group (P-value = 0.0001). Dysphagia, early satiation, and nausea significantly reduced in the drug group while the placebo group showed no improvement. Our results suggest that constipation, bloating, belching, and odynophagia did not significantly improve in none of the groups.

Conclusion: This study showed that Habb-e-Mastaki is effective against GERD. Further detailed in vitro and in vivo studies aimed at discovering the mechanism of action of this formulation and clinical studies involving a larger population will be necessary to explain and confirm the results obtained in the present study.

Methods: The level of sister chromatid exchanges (SCEs) and chromosomal aberrations (CAs) were measured in cultured human blood lymphocytes treated with cisplatin and/or vitamin B12.

Results: The results showed a significantly elevated frequency of CAs and SCEs of cisplatin-treated cultures compared to the control (P < 0.05). The CAs and SCEs induced by cisplatin were significantly lowered by pretreatment of cell cultures with vitamin B12. In addition, cisplatin caused a slight reduction in the mitotic index (MI), while vitamin B12 did not modulate the effect of cisplatin on MI.

Conclusion: Vitamin B12 can protect human lymphocytes against genotoxicity associated with cisplatin.

Methods: To achieve this, a comprehensive search was conducted in Persian medicine references and scientific databases to gather information on the traditional uses, chemical composition, and pharmacological effects of spinach. Studies that met the inclusion criteria were meticulously categorized, and relevant data were analyzed to draw insightful comparisons.

Results: Persian medicine describes spinach as a nutrient-rich, laxative, and fast-digesting agent with therapeutic effects on inflammation, lung diseases, back pain, sore throats, jaundice, urinary disorders, joint pain, eye inflammation, insomnia, dementia, and more. Modern studies have substantially corroborated these traditional uses, revealing that spinach possesses antioxidant, anti-inflammatory, anti-cancer, blood sugar-lowering, lipid-lowering, anti-obesity, neurological, ocular, and musculoskeletal effects.

Conclusion: Spinach exhibits a wide range of beneficial effects on various health conditions. Its widespread availability, low cost, and exceptional nutritional richness position it as a promising candidate for further investigation. Future studies should explore the clinical effectiveness of spinach in various diseases, while taking into consideration the principles emphasized in Persian medicine to guide research and inform therapeutic strategies.

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.

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.

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.

Methods: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to analyze the inhibitory effect of raltitrexed on cell proliferation. The effect of raltitrexed on radiosensitivity was studied through a clone-forming experiment. The scratch assay and invasion test were performed to understand the cell migration and invasion abilities. The apoptosis rate change was measured using a flow cytometer, and Western Blotting was used to determine the expression of B cell lymphoma-2 (Bcl-2) and Bcl2-associated X protein (Bax) in each group.

Results: Raltitrexed significantly inhibited ECA109 proliferation in a time-dose-dependent manner; there were significant differences among different concentrations and times of action. The results of the clone-forming experiment showed a sensitization enhancement ratio of 1.65, and this demonstrated a radiosensitization effect. After the combination of raltitrexed with X-ray, the cell migration distance was shortened, and the number of cells penetrating the membrane was reduced.

Conclusion: Raltitrexed can inhibit the growth of esophageal cancer ECA109 cells and has a radiosensitization effect.

Methods: We conducted a comprehensive analysis of the expression of SLC7A11 across 33 cancer types, employing datasets from public databases. Methods, such as Cox regression and survival analyses assessed its prognostic significance, while functional enrichment explored the biological processes tied to SLC7A11. The association between SLC7A11 expression, immune cell infiltration, and immune-related gene expression was also scrutinized.

Results: Notably, SLC7A11 expression was more pronounced in cancerous compared to normal samples and correlated with higher tumor grades. Increased SLC7A11 expression was linked to poor outcomes, particularly in liver hepatocellular carcinoma (LIHC). This protein's expression also showcased significant relationships with diverse molecular and immune subtypes.

Additionally, a prognostic nomogram was devised, integrating SLC7A11 expression and clinical variables. High SLC7A11 levels corresponded with cell growth and senescence pathways in various cancers and with lipid and cholesterol metabolism in LIHC. Furthermore, potential therapeutic compounds for LIHC with high SLC7A11 were identified. Real-time PCR (qPCR) and Western blot were conducted to explore the expression of SLC7A11 in tumor tissues and cancer cell lines.

Conclusion: In summation, this study emphasizes the prognostic and immunological importance of SLC7A11, spotlighting its potential as a therapeutic target in LIHC.

Objective: We herein summarize additional sources of DPD enzyme activity variability, spanning from epigenetic regulation of DPYD expression, factors potentially inducing protein modifications, as well as drug-enzyme interactions that contribute to fluoropyrimidine toxicity.

Results: While seminal in vitro studies provided evidence that DPYD promoter methylation downregulates DPD expression, the association of DPYD methylation with fluoropyrimidine toxicity was not replicated in clinical studies. Different non-coding RNA molecules, such as microRNA, piwi-RNAs, circular-RNAs and long non-coding RNAs, are involved in post-transcriptional DPYD regulation. DPD protein modifications and environmental factors affecting enzyme activity may also add a proportion to the pooled variability of DPD enzyme activity. Lastly, DPD-drug interactions are common in therapeutics, with the most well-characterized paradigm the withdrawal of sorivudine due to fluoropyrimidine toxicity deaths in 5-FU treated cancer patients; a mechanism involving DPD severe inhibition.

Conclusions: DPYD polymorphisms are the main source of DPD variability. A study on DPYD epigenetics (both transcriptionally and post-transcriptionally) holds promise to provide insights into molecular pathways of fluoropyrimidine toxicity. Additional post-translational DPD modifications, as well as DPD inhibition by other drugs, may explain a proportion of enzyme activity variability. Therefore, there is still a lot we can learn about the DPYD/DPD fluoropyrimidine-induced toxicity machinery.

Methods: A novel Electrochemiluminescence (ECL) immunoassay for the quantitation of PYX- 106 in human serum was developed and validated. Biotinylated anti-PYX-106 antibody Bio-A1A1 was employed as the capture antibody, and ruthenylated anti-PYX-106 antibody Ru-A3G10 was utilized as the detection antibody in the ECL immunoassay on Meso Scale Discovery (MSD) platform.

Results: This assay was fully validated in terms of selectivity, accuracy, precision, hook effect, stability, etc., with a dynamic range from 50.0 to 2,500 ng/mL in human serum under the 2018 U.S. Food and Drug Administration (FDA) guidance and the 2022 U.S. FDA ICH M10 guidance.

Conclusion: PYX-106 bioanalytical assay validation was reported for the first time in a biological matrix, and this assay has been successfully applied to support a clinical trial PYX-106-101.

Aim: To clarify the mechanism of HDW for esophageal adenocarcinoma (EAC), we utilized network pharmacology and weighted gene co-expression network analysis methods (WGCNA).

Methods: The gene modules that were linked with the clinical features of EAC were obtained through the WGCNA method. Then, the potential target genes were retrieved through the network pharmacology method in order to determine the targets of the active components. After enrichment analysis, a variety of signaling pathways with significant ratios of target genes were found, including regulation of trans-synaptic signaling, neuroactive ligand-receptor interaction and modulation of chemical synaptic transmission. By means of protein-protein interaction (PPI) network analysis, we have successfully identified the hub genes, which were AR, CNR1, GRIK1, MAPK10, MAPT, PGR and PIK3R1.

Result: Our study employed molecular docking simulations to evaluate the binding affinity of the active components with the hub gene. The identified active anticancer constituents in HDW are scopoletol, quercetin, ferulic acid, coumarin, and trans-4-methoxycinnamyl alcohol.

Conclusion: Our findings shed light on the molecular underpinnings of HDW in the treatment of EAC and hold great promise for the identification of potential HDW compounds and biomarkers for EAC therapy.

Objective: The present study aims to enhance understanding of the disease mechanism and its progression by identifying prognostic biomarkers, potential drug targets, and candidate drugs that can be used for therapy in pancreatic cancer.

Methods: Gene expression profiles from the GEO database were analyzed to identify reliable prognostic markers and potential drug targets. The disease's molecular mechanism and biological pathways were studied by investigating gene ontologies, KEGG pathways, and survival analysis to understand the strong prognostic power of key DEGs. FDA-approved anti-cancer drugs were screened through cell line databases, and docking studies were performed to identify drugs with high affinity for ARNTL2 and PIK3C2A. Molecular dynamic simulations of drug targets ARNTL2 and PIK3C2A in their native state and complex with nilotinib were carried out for 100 ns to validate their therapeutic potential in PDAC.

Results: Differentially expressed genes that are crucial regulators, including SUN1, PSMG3, PIK3C2A, SCRN1, and TRIAP1, were identified. Nilotinib as a candidate drug was screened using sensitivity analysis on CCLE and GDSC pancreatic cancer cell lines. Molecular dynamics simulations revealed the underlying mechanism of the binding of nilotinib with ARNTL2 and PIK3C2A and the dynamic perturbations. It validated nilotinib as a promising drug for pancreatic cancer.

Conclusion: This study accounts for prognostic markers, drug targets, and repurposed anti-cancer drugs to highlight their usefulness for translational research on developing novel therapies. Our results revealed potential and prospective clinical applications in drug targets ARNTL2, EGFR, and PI3KC2A for pancreatic cancer therapy.

Objective: To explore the inhibitory effect of combination treatment with SHR6390 and cabozantinib in HCC, and its antitumor mechanism, so as to provide a more effective therapeutic strategy for HCC patients.

Methods: We investigated SHR6390, monotherapy or combined with cabozantinib, by CCK8, wound healing, transwell, western blotting, immunohistochemistry and mouse model of a subcutaneous tumor.

Results: Our results show that SHR6390 exhibited potent anti-proliferative activity against HCC in a dose-dependent manner. SHR6390 combined with cabozantinib exhibited more potent inhibition of cell viability, migration and invasion. In terms of potential mechanisms, we found that cabozantinib could lead to phosphorylation of Rb, which was reduced in SHR6390 and combined groups. SHR6390 monotherapy inhibited the growth of subcutaneous HCC tumors, besides, the combination treatment with SHR6390 and cabozantinib exerted synergistic anti-tumor activity in vivo

Conclusion: SHR6390 is effective against HCC, monotherapy or combined with cabozantinib.

Methods: Bioinformatics analyses were employed to clarify TRIP13 expression in CRC tissues and predict the correlation of the TRIP13 enrichment pathway with glycolysis-related genes and stemness index mRNAsi. Quantitative real-time polymerase chain reaction and western blot were adopted to analyze the expression of TRIP13 and glycolysis- related genes. Cell Counting Kit-8 was utilized to determine the cell viability and IC₅₀ value. Western blot was employed to measure the expression of stemness-related factors. Cell function assays were performed to detect cells' sphere-forming ability and glycolysis level. Animal models were constructed to determine the effects of TRIP13 expression on CRC tumor growth.

Results: TRIP13 was significantly overexpressed in CRC, concentrated in the glycolysis signaling pathway, and positively correlated with stemness index mRNAsi. High expression of TRIP13 facilitated DOX resistance in CRC. Further mechanistic studies revealed that overexpression of TRIP13 could promote cell stemness through glycolysis, which was also confirmed in animal experiments.

Conclusion: TRIP13 was highly expressed in CRC, which enhanced the DOX resistance of CRC cells by activating glycolysis to promote cell stemness. These findings offer new insights into the pathogenesis of DOX resistance in CRC and suggest that TRIP13 may be a new target for reversing DOX resistance in CRC.

Methods: The expression of miR-488-3p was examined in normal human osteoblasts and OS cell lines (U2OS, Saos2, and OS 99-1) using RT-qPCR. U2OS cells were transfected with miR-488- 3p-mimic, and cell viability, apoptosis, migration, and invasion were assessed using CCK-8, flow cytometry, and Transwell assays, respectively. Western blotting and immunofluorescence were employed to measure apoptosis- and autophagy-related protein levels, as well as the autophagosome marker LC3. The binding sites between miR-488-3p and neurensin-2 (NRSN2) were predicted using online bioinformatics tools and confirmed by a dual-luciferase assay. Functional rescue experiments were conducted by co-transfecting miR-488-3p-mimic and pcDNA3.1-NRSN2 into U2OS cells to validate the effects of the miR-488-3p/NRSN2 axis on OS cell behaviors. Additionally, 3-MA, an autophagy inhibitor, was used to investigate the relationship between miR- 488-3p/NRSN2 and cell apoptosis and autophagy.

Results: miR-488-3p was found to be downregulated in OS cell lines, and its over-expression inhibited the viability, migration, and invasion while promoting apoptosis of U2OS cells. NRSN2 was identified as a direct target of miR-488-3p. Over-expression of NRSN2 partially counteracted the inhibitory effects of miR-488-3p on malignant behaviors of U2OS cells. Furthermore, miR- 488-3p induced autophagy in U2OS cells through NRSN2-mediated mechanisms. The autophagy inhibitor 3-MA partially reversed the effects of the miR-488-3p/NRSN2 axis in U2OS cells.

Conclusion: Our findings demonstrate that miR-488-3p suppresses malignant behaviors and promotes autophagy in OS cells by targeting NRSN2. This study provides insights into the role of miR-488-3p in OS pathogenesis and suggests its potential as a therapeutic target for OS treatment.

Methods: By setting the search terms correlated to PD-L1 and gastric cancer, a nearly comprehensive search was carried out in four major databases, and the deadline for searching was September 1, 2022. The retrieved documents were further screened by strict inclusion and exclusion criteria after removing the duplication. Next, the quality of the included studies was evaluated with the Newcastle-Ottawa Scale (NOS) scale. Finally, the STATA15.1 software was used to process data and draw plots, and the odds ratios (ORs) were adopted to assess the pooled effect size.

Results: A total of 85 works of literature were included in this study through screening strictly, and detailed data were extracted after evaluating the quality of the literature. The process of analysis was conducted in the whole population, Asia-Africa population, European and American population, and Asian population with CPS≥1, amd all found that the expression of PD-L1 in gastric cancer was correlated with age, tumor size, EBV infection, Her-2 expression and microsatellite status. However, the subgroup of the region also found some differences in Asian and Western regions, which was interesting and worth studying further. The included research of this study did not have significant publish bias.

Conclusion: After careful analysis, this study found that age (>60 years), tumor size (>5cm), EBV infection (+), Her-2 expression (+), microsatellite status (MSI), and mismatch repair status (dMMR) were risk factors for positive expression of PD-L1 in gastric cancer.

Background: IL1R2, a special member of IL-1 receptor family, binds to IL-1 and plays an important role in inhibiting IL-1 pathway, which seems to be involved in tumorigenesis. Emerging studies demonstrated higher IL1R2 expression levels in several malignancies.

Objective: In the present study, we assessed the expression of IL1R2 in LUAD tissues with immunohistochemistry and explored various databases to determine whether it could be a potential prognostic biomarker and therapeutic target.

Methods: The expression level of IL1R2 in lung adenocarcinoma was analyzed by Immunohistochemistry and UALCAN database. The correlation between IL1R2 expression and the patient prognosis was identified by Kaplan-Meier plotter. The correlation of IL1R2 expression with immune infiltrates was clarified by TIMER database. The protein-protein interaction network and gene functional enrichment analysis were constructed and performed by STRING and Metascape database.

Results: Immunohistochemistry showed that the expression of IL1R2 was higher in tumor tissues of LUAD patients and that patients with lower IL1R2 level have a better prognosis than their counterparts. We validated our findings in several online databases and found that IL1R2 gene was also positively correlated with B cells and neutrophils and biomarkers of CD8⁺T cells and exhausted T cells. PPI network and gene enrichment analyses showed that expression of IL1R2 was also associated with complex functionspecific networks involving IL-1 signal, NF-KappaB transcription factors.

Conclusion: According to these findings, we demonstrated that IL1R2 was involved in the progression and prognosis of LUAD and the underlying mechanism needs further investigation.

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.

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.

Conclusions: Our findings revealed the LINC00982/miR-183-5p/ABCA8 axis as a potential therapeutic target in LUAD.

Objective: Abuse of alcohol does not occur suddenly. People becoming addicted to various alcoholic beverages is a problem that results from months and years of irresponsible drinking. The process of recovering from the issue in turn includes targeted, particular methods for raising awareness of the negative effects of alcohol usage.

Conclusion: Due to the heightened risks for one's bodily and mental health along with the social issues it generates, alcohol consumption results in these costs. We discuss the three areas of the epidemiology of alcohol's impact on health and diseases, the public health approach for treating problems related to alcohol use, and advancements in alcohol science.

Background: STAD is a common diagnosed gastrointestinal malignancy and its heterogeneity is a big challenge that influences prognosis and precision therapies. Present study was designed to classify molecular subtypes and construct a prognostic gene signature based on miRNAs for the prognostic prediction and therapeutic response in STAD.

Objective: The objective of this study is to investigate the molecular subtypes and prognostic model for STAD.

Methods: A STAD specific miRNA-messenger RNA (mRNA) competing endogenous RNA (ceRNA) network was generated using the RNA-Seq and miRNA expression profiles from The Cancer Genome Atlas (TCGA) database, in which miRNA-related mRNAs were screened. Molecular subtypes were then determined using miRNA-related genes. Through univariate Cox analysis and multivariate regression analysis, a prognostic model was established in GSE84437 Train dataset and validated in GSE84437 Test, TCGA, GSE84437 and GSE66229 datasets. Immunotherapy datasets were employed for assessing the performance of the risk model. Finally, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was applied to validate the expression of hub genes used for the risk score signature.

Results: We constructed a ceRNA network containing 84 miRNAs and 907 mRNAs and determined two molecular subtypes based on 26 genes from the intersection of TCGASTAD and GSE84437 datasets. Subtype S2 had poor prognosis, lower tumor mutational burden, higher immune score and lower response to immunotherapy. Subtype S1 was more sensitive to Sorafenib, Pyrimethamine, Salubrinal, Gemcitabine, Vinorelbine and AKT inhibitor VIII. Next, a five-gene signature was generated and its robustness was validated in Test and external datasets. This risk model also had a good prediction performance in immunotherapy datasets.

Conclusion: This study promotes the underlying mechanisms of miRNA-based genes in STAD and offers directions for classification. A five-gene signature accurately predicts the prognosis and helps therapeutic options.

Methods: First, we typed cases from the TCGA-HNSC cohort into subtypes by a Bayesian non-negative matrix factorization (BayesNMF)-based consensus clustering approach. Subsequently, genomic and proteomic data from HNSC cell lines were integrated to identify biomarkers of response to targeted therapies and immunotherapies. Finally, associations between HNSC subtypes and CD8 T-cell-associated effector molecules, common immune checkpoint genes, were compared to assess the potential of HNSC subtypes as clinically predictive immune checkpoint blockade therapy.

Results: The 500 HNSC cases from TCGA were put through a consensus clustering approach to identify six HNSC expression subtypes. In addition, subtypes with unique proteomics and dependency profiles were defined based on HNSC cell line histology and proteomics data. Subtype 4 (S4) exhibits hyperproliferative and hyperimmune properties, and S4-associated cell lines show specific vulnerability to ADAT2, EIF5AL1, and PAK2. PD-L1 and CASP1 inhibitors have therapeutic potential in S4, and we have also demonstrated that S4 is more responsive to immune checkpoint blockade therapy.

Conclusion: Overall, our HNSC typing approach identified robust tumor-expressing subtypes, and data from multiple screens also revealed subtype-specific biology and vulnerabilities. These HNSC expression subtypes and their biomarkers will help develop more effective therapeutic strategies.

Methods: Using electronic databases, including PubMed, Embase, and EBSCO, a thorough literature search was carried out for the years 2006 to 2023. The search strategy was designed to identify relevant studies based on chemoimmunotherapy and chemotherapy intervention, and the search was conducted using appropriate keywords and MeSH terms. The retrieved studies were screened for relevance based on their titles, abstracts, and full texts. The studies' inclusion criteria were predefined, and the selected studies were then subjected to a quality assessment using GradePro GDT. The data from selected studies were extracted and analyzed using Revman version 5.4.

Results: The study found that chemoimmunotherapy treatment resulted in a significant improvement in overall survival (OS) with a risk ratio (RR) of 1.54 and a 95% Confidence Interval (CI) of 1.25 to 1.89. The overall effect was also found to be significant, with a p-value of less than 0.001. Furthermore, we also observed an improvement in the 1-year, 3-year, and 5-year survival rates with risk ratio (RR) of 1.09 (95% CI: 1.01, 1.17), 1.43 (95% CI: 1.28, 1.60), and 1.59 (95% CI: 1.10, 2.30), respectively. In addition, it’s also found that chemoimmunotherapy treatment also resulted in an improvement in DFS with an RR of 1.94 and a 95% CI of 1.44 to 2.59. Overall, these results suggest that chemoimmunotherapy treatment can be an effective approach in comparison to chemotherapy for improving overall survival and disease-free survival in the studied population.

Conclusion: This study comparing chemoimmunotherapy versus chemotherapy for gastric cancer showed that both treatments were effective, but chemoimmunotherapy had more significant efficacy. To support these results, additional studies with a large sample size and a longer follow-up time are required.

Methods: Bioinformatics was used to analyze the relationship between CBX8 level and tumor and the enrichment pathway of CBX8 enrichment. qRT-PCR was used to detect the differential expression of CBX8 in LC cells and normal lung epithelial cells. The effects of knockdown or overexpression of CBX8 on the proliferation, migration and invasion of LC cells were evaluated by CCK- -8 assay and Transwell assay, and the levels of proteins associated with the EMT pathway and Wnt/ β-catenin signaling pathway were detected by western blot.

Results: Bioinformatics analysis revealed that CBX8 was highly expressed in LC and enriched on the Wnt/β-catenin signaling pathway. The expression level of CBX8 was significantly elevated in LC cells. Knockdown of CBX8 significantly inhibited cell proliferation, migration and invasion, and decreased the expression levels of EMT-related proteins and Wnt/β-catenin pathway-related proteins. Conversely, overexpression of CBX8 promoted cell proliferation, migration and invasion, and increased the expression levels of EMT-related proteins and Wnt/β-catenin pathway-related proteins. The Wnt inhibitor IWP-4 alleviated the effects produced by overexpression of CBX8.

Conclusion: Collectively, these data demonstrated that CBX8 induced EMT through Wnt/β-- catenin signaling, driving migration and invasion of LC cells.

Objective: This study aims to review and summarize the published literature regarding LA in the treatment of benign and malignant thyroid nodules.

Methods: A comprehensive literature search on PubMed from 2000 to 2023 was carried out. The search terms included: thyroid, nodules, laser, cancer, lymph node metastasis, and autonomously functioning nodules. The most relevant investigations in the field were selected.

Results: In the last two decades, a very remarkable number of papers consistently demonstrated that LA is able to durably shrink benign nodules on average by about 50%; better results are obtained in spongiform nodules with a volume less than 15 ml; 500 J/ml of tissue should be administered. LA may be a valid option to treat autonomously functioning nodules and papillary thyroid cancers especially if they are <10 mm, and with neck recurrence in patients already submitted to surgery. LA has also been demonstrated to be cost-effective compared to surgical treatment both in benign and malignant lesions, with similar outcomes.

Conclusion: Evidence demonstrated that LA is a valid alternative to surgery in benign and malignant thyroid lesions, but also to obtain a successful treatment, a careful selection of the lesion is mandatory.

Benzimidazole scaffold is an exclusive structure in drug design and discovery. Many new pharmaceutical drugs containing benzimidazole are anticipated to be available within the next ten years as a result of the extensive therapeutic applications of benzimidazole and its derivatives. This review inspired many researchers to develop more biologically active compounds bearing benzimidazole, expanding the scope of finding a remedy for other diseases. From this study, we concluded that 2-substituted benzimidazole was considered more extensively by researchers.

Methods: Using the TCGA (The Cancer Genome Atlas), the GEO (Gene Expression Omnibus) dataset, and multiple bioinformatic tools, we investigated the function of PRSS27 in 33 tumor types. In addition, prognosis analysis of PRSS27 in breast cancer was carried out, as well as in vitro experiments to verify its role as an oncogene. We first explored the expression of PRSS27 in over 10 tumors and then we looked into PRSS27 genomic mutations.

Results: We discovered that PRSS27 has prognostic significance in breast cancer and other cancers' survival, and we developed a breast cancer prognostic prediction model by combining a defined set of clinical factors. Besides, we confirmed PRSS27 as an oncogene in breast cancer using some primary in vitro experiments.

Conclusion: Our pan-cancer survey has comprehensively reviewed the oncogenic function of PRSS27 in various human malignancies, suggesting that it may be a promising prognostic biomarker and tumor therapeutic target in breast cancer.

Methods: GSE23558 and GSE52130 data sets were selected, and differential gene expression analysis was performed using microarray data from GSE52130 and GSE23558. The analysis focused on comparing OLP and OSCC samples with normal samples. The genes intersected through the differential gene expression analysis were then extracted to determine the overlapping genes among the upregulated or downregulated DEGs. The downregulated genes among the DEGs were subsequently imported into the miRWalk database to search for potential target genes of miRNA 483-5p that lacked validation. To gain insight into the biological pathways associated with the DEGs, we conducted pathway analysis utilizing tools, such as Enrichr. Additionally, the cellular components associated with these DEGs were investigated by analyzing the String database. On the other hand, blood serum samples were collected from 35 OSCC patients, 34 OLP patients, and 34 healthy volunteers. The expression level of miR-483-5p was determined using quantitative reverse transcription polymerase chain reaction (RT-qPCR). The Kruskal-Wallis test was utilized to investigate the considerable correlation. Moreover, this study explored the prognostic value of miR-483-5p through its association with clinicopathological parameters in OSCC patients.

Results: The results showed that serum expression of miR-483-5p was considerably higher in OSCC patients compared to OLP patients and healthy controls (p 0.0001) and that this difference was statistically significant. Furthermore, elevated miR-483-5p expression was associated with tumor size, lymph node metastasis, and stage of tumor nodal metastasis in OSCC patients (p 0.001, p 0.038, and p 0.0001, respectively). In silico analysis found 71 upregulated genes at the intersection of upregulated DEGs and 44 downregulated genes at the intersection of downregulated DEGs, offering insight into the potential underlying mechanisms of miR-483-5p’s engagement in OSCC and OLP. The majority of these DEGs were found to be involved in autophagy pathways, but DEGs involved in the histidine metabolism pathway showed significant results. Most of these DEGs were located in the extracellular region. After screening for downregulated genes that were invalidated, miRNA 483-5p had 7 target genes.

Conclusion: This study demonstrates the potential of serum miR-483-5p as a promising diagnostic and prognostic biomarker in OSCC and OLP patients. Its upregulation in OSCC patients and its association with advanced tumor stage and potential metastasis suggest the involvement of miR-483-5p in critical signaling pathways involved in cell proliferation, apoptosis, and cell cycle regulation, making it a reliable indicator of disease progression. Nevertheless, additional experimental studies are essential to validate these findings and establish a foundation for the advancement of targeted therapies and personalized treatment approaches.

Methods: Biological potential of hinokiflavone in medicine have been analyzed in the present work through scientific data analysis of various literature work. Scientific database, including Google, Scopus, Science Direct, and PubMed were searched to collect all the scientific information of the present work using terms flavonoid, biflavonoid, herbal medicine, and hinokiflavone. Pharmacological activities of hinokiflavone were analyzed in the present work in very detailed manner. Analytical data of hinokiflavone were collected and analyzed in present work in order to know the biological source of hinokiflavone.

Results: Present work signified the biological importance of hinokiflavone against various types of cancerous disorders, including breast cancer, colorectal cancer, esophageal squamous cancer, adenocarcinoma, hepatocellular carcinoma, myeloid leukemia, and melanoma. Further, its antiinflammatory, hepatoprotective, anti-viral, and anti-oxidant potential were also discussed in the present work. Moreover, its biological potential against COVID-19 and hair loss, and procoagulant activity were also summarized in this paper. Analytical data on hinokiflavone signified the importance of various analytical techniques in the extraction, separation, and identification of hinokiflavone with their pharmacokinetic parameters.

Conclusion: Present work signified the biological importance and therapeutic potential of hinokiflavone in medicine.

Objective: The objective of the study was to analyze and validate the metabolic abnormalities and the role of MTCI in esophageal squamous cell carcinoma.

Methods: In this work, we collected transcriptomic data from 160 esophageal squamous carcinoma samples and 11 normal tissue samples from The Cancer Genome Atlas (TCGA). The OmicsBean and GEPIA2 were used to conduct an analysis of differential gene expression and survival in clinical samples. Rotenone was used to inhibit the MTCI activity. Subsequently, we detected lactate production, glucose uptake, and ATP production.

Results: A total of 1710 genes were identified as being significantly differentially expressed. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis suggested that these differentially expressed genes (DEGs) were significantly enriched in various pathways related to carcinoma tumorigenesis and progression. Moreover, we further identified abnormalities in metabolic pathways, in particular, the significantly low expression of multiple subunits of MTCI genes (ND1, ND2, ND3, ND4, ND4L, ND5, and ND6). Rotenone was used to inhibit the MTCI activity of EC109 cells, and it was found that the decrease in MTCI activity promoted HIF1A expression, glucose consumption, lactate production, ATP production, and cell migration.

Conclusion: Our results indicated the occurrence of abnormal metabolism involving decreased mitochondrial complex I activity and increased glycolysis in esophageal squamous cell carcinoma (ESCC), which might be related to its development and degree of malignancy.

Methods: Three different categories of allopathy and ayurvedic medicines, such as antacids (omeprazole, ranitidine, and sooktybhasma), antibacterial (amoxicillin trihydrate, ciprofloxacin hydrochloride, Curcuma longa, and Datura stramonium) and antiviral (acyclovir, efavirenz, Echinacea, Calendula, Allium sativum, and Citrullus colocynthis) were targeted.

Results: Best therapeutic hybrid combination was obtained on the basis of their UV absorption maxima and peak shift. Acyclovir with A. sativum (1-6%), sooktybhasma 20% with rantidine, Ciprofloxacin HCl (2%) with 10% aqueous datura and Ciprofloxacin HCl (0.02-0.2%) with 0.02-0.06% acetonitrile turmeric showed best integration result. This drug integration can be applied to improve the potential results or detoxification of hybrid drugs that target the drug moiety results in reduced side effects or the dose of important drugs, which might be due to the chelation pattern of their functional group, absorption, bonding, and pi-pi interaction.

Conclusion: This study will provide the leadership for the betterment of a therapeutic hybrid drug complex that might be useful as an allopathic drug and less harmful than its ayurvedic component. The proposed integration fusion of different medication therapies, such as Ayurvedic and allopathic, has the potential for a scientific merger.

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.

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.

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.

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.

Method: Thus, identifying biomarkers to predict recurrence is crucial. In our study, we analyzed data from CCLE, GEO, and TCGA, identifying eight oncogenes associated with HCC. Subsequently, the expression of 8 genes was tested in 5 cases of tumor tissues and the adjacent non-tumor tissues. Then ATP6AP1, PSMD14 and HSP90AB1 were selected to verify the expression in 63 cases of tumor tissues and the adjacent non-tumor tissues. The results showed that ATP6AP1, PSMD14, HSP90AB1 were generally highly expressed in tumor tissues. A five-year follow-up of the 63 clinical cases, combined with Kaplan-Meier Plotter's relapse-free survival (RFS) analysis, found a significant correlation between PSMD14 expression and recurrence in HCC patients. Subsequently, we analyzed the PSMD14 mutations and found that the PSMD14 gene mutations can lead to a shorter disease-free survival time for HCC patients.

Results: The results of enrichment analysis indicated that the differentially expressed genes related to PSMD14 are mainly enriched in the signal release pathway.

Conclusion: In conclusion, our research showed that PSMD14 might be related to recurrence in HCC patients, and the expression of PSMD14 in tumor tissue might be a potential prognostic biomarker after tumor resection in HCC patients.

Observations: Natural origin, low in vivo toxicity, and pleiotropic functional essence are the foremost fascinations for HST use as an anticancer drug. However, low aqueous solubility accompanied with a prompt degradation by intestinal and hepatocellular enzymes impairs HST physiological absorption.

Motivation: Remedies attempted herein comprise the synthesis of derivatives and nanocarrier (NC)-mediated delivery. As the derivative synthesis aggravates the structural complexity, NC-driven HST delivery has emerged as a sustainable approach for its sustained release. Recent interest in HST has been due to its significant anticancer potential, characterized via inhibited cell division (proliferation), new blood vessel formation (angiogenesis), forceful occupation of neighboring cell’s space (invasion), migration to erstwhile physiological locations (metastasis) and apoptotic induction. The sensitization of chemotherapeutic drugs (CDs) by HST is driven via stoichiometrically regulated synergistic actions.

Purpose and Conclusion: This article sheds light on HST structure-function correlation and pleiotropic anticancer mechanisms, in unaided and NC-administered delivery in singular and with CDs synergy. The discussion could streamline the HST usefulness and long-term anticancer efficacy.

Methods: In this study, we examined JNK2 expression in patient samples and performed experiments involving the knockdown and inhibition of the JNK2 in ESCC cell lines.

Results: Higher JNK2 expression was observed in tumor tissues compared to adjacent tissues. JNK2 overexpression was associated with advanced disease stages and poor prognosis. Furthermore, knockdown or inhibition of JNK2 in ESCC cell lines resulted in a decrease in cell proliferation and migration.

Conclusion: Additionally, a significant decrease in the expression of β-catenin and vimentin, along with an increase in the expression of Axin2, was observed upon downregulation of JNK2. Our study provides insight into the role of JNK2 in ESCC and its potential regulatory mechanism, offering a potential therapeutic strategy for ESCC patients with aberrant JNK2 expression.

Objective: This study aimed to evaluate the nutritional value and physical quality of purple sweet potato-based ONS.

Methods: A new local food-based formula was formulated by using purple sweet potato as the main ingredient. This new formula, which was then mentioned as the treatment formula, was subsequently compared with the control formula. The control formula was made from ingredients commonly used for producing ONS in hospitals in Indonesia, such as milk powder, sugar, oil, and other additives such as maltodextrin and creamer. Meanwhile, the treatment formula was labelled into three treatment formulas based on the differences in the proportions of white egg flour and whey protein as a protein source in each treatment formula. The treatment formula was formulated by using local ingredients of purple sweet potato flour and egg white flour by adding whey protein, extra virgin olive oil, omega-3 powder, sugar, and creamer. A proximate analysis was conducted to analyze the nutrient content of the formula and the viscosity and osmolarity tests were conducted to evaluate the physical qualities of the formula. The laboratory analysis results were described as descriptive data, then analyzed by using One-Way ANOVA. The determination of the best treatment formula in the form of effectiveness (Nh).

Results: The results of the proximate test and physical quality showed that the best formula based on the highest Nh value of 0.75 was P3 with 245 kcal energy, 8.8 g (14%) protein, 6.5 g (24%) fat, and 37.8 g (62%) carbohydrate, viscosity 28.1 cP, and osmolarity 492.3 mOsm (iso-osmolar) per serving size (200 ml).

Conclusion: Formula P3 which contains more egg white flour than whey protein is the best formula that has the best nutritional value and good physical quality.

Objective: This study aimed to explore the embedding mechanism of FAM83H-AS1 molecules in terms of radio sensitivity of LC and provide potentially effective therapeutic targets for LC therapy.

Methods: Quantitative real-time PCR (qRT-PCR) was conducted to measure the transcription levels of genes. Proliferation was determined via CCK8 and colony formation assays. Western blot was carried out to detect the relative protein expression. A xenograft mouse model was constructed to investigate the effect of LncRNA FAM83H-AS1 on tumor growth and radio-sensitivity in vivo.

Results: The levels of lncRNA FAM83H-AS1 were remarkably increased in LC. Knockdown of FAM83H-AS1 inhibited LC cell proliferation and colony survival fraction. Deletion of FAM83H-AS1 increased the sensitivity of LC cells to 4 Gy of X-ray radiation. In the xenograft model, radiotherapy combined with FAM83H-AS1 silencing significantly reduced tumor volume and weight. Overexpression of FAM83H reversed the effects of FAM83H-AS1 deletion on proliferation and colony survival fraction in LC cells. Moreover, the over-expressing of FAM83H also restored the tumor volume and weight reduction caused by the knockdown of FAM83H-AS1 or radiation in the xenograft model.

Conclusion: Knockdown of lncRNA FAM83H-AS1 inhibited LC growth and enhanced radiosensitivity in LC. It has the potential to be a promising target for LC therapy.