Harris C C
Laboratory of Human Carcinogenesis, Division of Basic Science, National Cancer Institute, Bethesda, MD 20892-4255, USA.
J Natl Cancer Inst. 1996 Oct 16;88(20):1442-55. doi: 10.1093/jnci/88.20.1442.
The p53 tumor suppressor protein is involved in multiple central cellular processes, including transcription, DNA repair, genomic stability, senescence, cell cycle control, and apoptosis. p53 is functionally inactivated by structural mutations, interaction with viral products, and endogenous cellular mechanisms in the majority of human cancers. This functional inactivation can, in some circumstances, produce resistance to DNA-damaging agents commonly used in cancer chemotherapy and radiotherapeutic approaches. Current research is defining the biochemical pathways through which p53 induces cell cycle arrest and apoptosis. Knowledge of these fundamental processes is leading to the identification of molecular targets toward which multimodality cancer therapies, using chemotherapeutic, immunotherapeutic, and gene-therapeutic strategies, can be based.
p53肿瘤抑制蛋白参与多种核心细胞过程,包括转录、DNA修复、基因组稳定性、衰老、细胞周期调控和细胞凋亡。在大多数人类癌症中,p53通过结构突变、与病毒产物的相互作用以及内源性细胞机制而功能失活。在某些情况下,这种功能失活会导致对癌症化疗和放射治疗中常用的DNA损伤剂产生抗性。目前的研究正在确定p53诱导细胞周期停滞和细胞凋亡的生化途径。对这些基本过程的了解正促使人们识别出分子靶点,基于这些靶点可以采用化疗、免疫治疗和基因治疗策略开展多模式癌症治疗。