作者: Xiang Gao , Kenneth V. Honn
DOI: 10.1016/S1569-254X(99)80006-5
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摘要: Publisher Summary This chapter discusses molecular biology of prostate cancer (PCa). Cancer arises from the accumulation several genetic mutations, including both mutations that activate dominant oncogenes and inactivate tumor suppressor genes. One most intensively studied genes are p53. Inactivation p53 protein by mutation, or its interactions with amplified cellular p53- associating (MDM2) viral proteins, can result in malignancy. Rb works at a different level same signaling pathway as p53, also mediate cell cycle G1 arrest. As understanding cell-cycle regulation increases, more powerful assays become available for assessing controls deficient specific cancers. Such characterization may not only dictate choice schedule currently existing phase- cycle-specific agents to be used therapy but lead an explosion novel mechanistic targets therapeutic intervention.