Abstract
AbstractA new approach to the modular, complex systems analysis of nonlinear dynamics of arrested neural cell Differentiation--induced cell proliferation during organismic development and the analogous cell cycling network transformations involved in carcinogenesis is proposed. Neural tissue arrested differentiation that induces cell proliferation during perturbed development and Carcinogenesis are complex processes that involve dynamically inter-connected biomolecules in the intercellular, membrane, cytosolic, nuclear and nucleolar compartments. Such 'dynamically inter-connected' biomolecules form numerous inter-related pathways referred to as 'molecular networks'. One such family of signaling pathways contains the cell cyclins. Cyclins are proteins that link several critical pro-apoptotic and other cell cycling/division components, including the tumor suppressor gene TP53 and its product, the Thomsen-Friedenreich antigen (T antigen), Rb, mdm2, c-Myc, p21, p27, Bax, Bad and Bcl-2, which play major roles in various neoplastic transformations of many tissues.The novel theoretical analysis presented here is based on recently published studies of arrested cell differentiation that normally leads to neural system formation during early developmental stages; the perturbed development may involve cyclin signaling and cell cycling responsible for rapidly induced cell proliferation without differentiation into neural cells in such experimental studies.
Highlights
A new approach to the modular, complex systems analysis of nonlinear dynamics in cell cycling network transformations involved in carcinogenesis is proposed
In human lung tumors and soft tissue sarcomas, it has recently been discovered that cyclin A/cdk2 complex expression and kinase activity were reliable predictors of proliferation and unfavorable prognosis, thereby further substantiating the epidemiological factors of cyclin signaling (Dobashi et al, 2003; Noguchi et al, 2000)
Regarding the molecular interaction between p27 and D-cyclin, CDK4 is a clear candidate as a mediating molecule (Bryja et al, 2004)
Summary
Cyclin E1 locus amplification is rare in breast cancer, the protein product is overexpressed in over 40% of breast carcinomas (Loden et al, 2002). Cyclin D1 is predominantly overexpressed in ERC tumors, and cyclin E overexpression is confined to ER¡ tumors (Gillett et al, 1994; Alle et al, 1998; Loden et al, 2002). The overexpression of several cell cycle regulators has been strongly associated with apoptotic-like behavior, as well as frank apoptosis, in cancer cells, which include c-Myc, E2F-1 and HPV. Apoptosis and its connection to cell cycle-related proteins is of interest therapeutically, as these types therapies could lead to the cancer cell annihilation via apoptosis. A shift has occurred, changing the focus of chemotherapy from exploration of agents that cause cell growth arrest to those that favor apoptosis
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