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癌细胞周期。

Cancer cell cycles.

作者信息

Sherr C J

机构信息

Howard Hughes Medical Institute, Department of Tumor Cell Biology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA.

出版信息

Science. 1996 Dec 6;274(5293):1672-7. doi: 10.1126/science.274.5293.1672.

Abstract

Uncontrolled cell proliferation is the hallmark of cancer, and tumor cells have typically acquired damage to genes that directly regulate their cell cycles. Genetic alterations affecting p16(INK4a) and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein (RB) and control exit from the G1 phase of the cell cycle, are so frequent 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 cell cycle per se, may participate in checkpoint functions that regulate homeostatic tissue renewal throughout life.

摘要

不受控制的细胞增殖是癌症的标志,肿瘤细胞通常在直接调节其细胞周期的基因上发生损伤。影响p16(INK4a)和细胞周期蛋白D1的基因改变在人类癌症中非常常见,这两种蛋白控制视网膜母细胞瘤蛋白(RB)的磷酸化并调控细胞周期G1期的退出,因此该信号通路的失活很可能是肿瘤发生所必需的。与肿瘤抑制蛋白p53一样,这条“RB信号通路”的组成部分虽然本身对细胞周期不是必需的,但可能参与了调节终身稳态组织更新的检查点功能。

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