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Foundations in Cancer Research p53 and ATM: Cell Cycle, Cell Death, and Cancer

1997; Elsevier BV; Linguagem: Inglês

10.1016/s0065-230x(08)60095-0

2162-5557

Susan E. Morgan, Michael B. Kastan,

Microtubule and mitosis dynamics

The chapter focuses on the current level of understanding of the roles both p53 and mutated in ataxia-telangiectasia (ATM) play in cell cycle control in response to DNA damage, and how alterations in these genes may contribute to tumorigenesis. The p53 tumor suppressor gene and the gene product ATM mediate cell cycle perturbations in response to DNA damage, and play a role in cell death, genetic stability, and cancer susceptibility. p53 is a critical participant in a signal transduction pathway that mediates either a G1 arrest or programmed cell death in response to DNA damage. In addition, p53 has been implicated to be an active component of a mitotic spindle checkpoint and a regulator of centrosome function. Inactivation of normal p53 function could thus result in inappropriate replication of damaged DNA, inappropriate cellular survival after cellular stresses, or abnormal segregation of chromosomes during mitosis, thus contributing to the malignant transformation of cells.