Proponent Specificity as Targeting Evolutionary Traits in Ras Isoform Mutability in Carcinogenesis

Abstract

Distributional and re-distributional patterns of compartmentalization of RAS isoforms are core, persistently active abnormalities that are central/additional phenomena within mutable molecular structure and dysfunction in carcinogenesis. In such terms, ongoing transformations attributes, both within the plasmalemma and the internal membrane compartments, potentiate transformation, as further illustrated by sequestration of mutational forms of RAS. The incremental adaptation response of injured cells further conforms with the resultant dimensions of cooperating networks, rather than as linear pathways; these network organizations induce groups of neoplastic cells to further augment the effector end-target predispositions toward pre-carcinogenesis and carcinogenesis. RAS formulation is hence primarily an effector initiator and maintenance-inducing role-pattern formulator in carcinogenesis, as reflected in central metabolic pathways of cell growth promotion and proliferation.