Canman C E, Kastan M B
Johns Hopkins Oncology Center, Baltimore, MD 21287, USA.
Semin Cancer Biol. 1995 Feb;6(1):17-25. doi: 10.1006/scbi.1995.0003.
The p53 tumor suppressor gene product, and the bcr-abl, bcl-2, and c-myc gene products all appear to influence the susceptibility of cells to apoptosis. In addition to the role p53 protein plays in mediating a cell cycle arrest in G1 following DNA damage, p53 also performs functions critical for removal of damaged cells by initiating apoptosis in certain physiological situations. Cells which express deregulated c-myc are sensitized to apoptosis following various growth suppressing stimuli and these observations have provided new insights into how apoptosis-suppressing genes such as mutant p53, bcl-2 and bcr-abl may cooperate during transformation and how they might influence the sensitivity of cells to radiation and chemotherapy.
p53肿瘤抑制基因产物以及bcr-abl、bcl-2和c-myc基因产物似乎均会影响细胞对凋亡的易感性。除了p53蛋白在介导DNA损伤后细胞周期停滞于G1期所发挥的作用外，p53在某些生理情况下通过启动凋亡对清除受损细胞也起着关键作用。表达失调的c-myc的细胞在各种生长抑制刺激后对凋亡敏感，这些观察结果为诸如突变型p53、bcl-2和bcr-abl等凋亡抑制基因在转化过程中如何协同作用以及它们如何影响细胞对放疗和化疗的敏感性提供了新的见解。
