  A new approach to the modular, complex systems analysis of nonlinear dynamics
in cell cycling network transformations involved in carcinogenesis is proposed.
Carcinogenesis is a complex process that involves dynamically inter-connected
biomolecules in the intercellular, membrane, cytosolic, nuclear and nucleolar
compartments that form numerous inter-related pathways. One such family of
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 all
play major roles in neoplastic transformation of many tissues. This novel
theoretical analysis based on recently published studies of cyclin signaling,
with special emphasis placed on the roles of cyclins D1 and E, suggests novel
clinical trials and rational therapies of cancer through reestablishment of
cell cycling inhibition in metastatic cancer cells.
