Untitled

Abstract

Significant participation of constitutive self-programming of apoptotic pathways indicates an in-built series of mechanistic pathways that protect against susceptibility patterns of evolving carcinogenesis. As such the incremental exposure pathways include dimensional re-formulation of events as wellestablished programmed schemes of network operability within the further conceptual realization of direct and indirect effects on cell viability once malignant transformation has taken place. Specific contexts of strict preconditioning and further stages of sustained conditions of cells such as seen in epithelial cells of breast and uterus come to operate in dominant fashion in determining cell-subset fate outcome when such cells are exposed to stress or injury. Chemotherapeutic resistance of malignant tumor cells would arise in terms of such contextual conditioning that includes in particular the genotype of the cells concerned. Mechanistic individualization of component intermediates of specific pathways is modulated in a manner that enhances such context of involvement of integral cells beyond the simple conformations of even interactive systems of effect and progression. Initial response of tumor cells to administered chemotherapeutic agents is supplemented by the development of second-stage resistance to such agents in many patients and would be indicative of adaptive low-metabolic status and non-proliferation of the tumor cells. In this setting, parameters of integration belie stratified re-organization of individual pathway mechanics and would implicate otherwise homeostatic countersystems that enhance pro-apoptosis or anti-apoptosis in response to radiation or chemotherapy of tumor cells.