Contrasting influence exerted by a chronicity of the acute inflammatory reactivity affecting
the colorectal mucosa in ulcerative colitis induces a progression in dysplasia as permissive
conditioning of the cellular microenvironment. Inducible representative models would allow the
emergence of a series of consequential pathways as identifiable profiles that project as carcinogenesis.
It is in terms of relatively simple dimensional increase in proliferative cellular activity that epithelial
cell dysplasia further promotes malignant transformation in the relative absence of corrective or
reparative gene expression systems. The increased potentiality for malignant change is symptomatic of
the progressiveness towards definable loss of fidelity of constitutive pathways that both specifically
and non-specifically contribute to pathobiology of carcinogenetic pathways as overlapping incomplete
profiles of preneoplastic and paraneoplastic integrative systems of reproducibility.
Keywords: proliferation, transformation, preneoplastic, paraneoplastic.
