CANCER CELL-CYCLES

Uncontrolled cell proliferation is the hallmark of cancer, and tumor c ells have typically acquired damage to genes that directly regulate th eir cell cycles. Genetic alterations affecting p16(INK4a) and cyclin D 1, proteins that govern phosphorylation of the retinoblastoma protein (RE) and control exit from the G(1) phase of the cell cycle, are so fr equent in human cancers that inactivation of this pathway may well be necessary for tumor development. Like the tumor suppressor protein p53 , components of this ''RB pathway,'' although not essential for the ce ll cycle per se, may participate in checkpoint functions that regulate homeostatic tissue renewal throughout life.