INDUCTION OF APOPTOSIS BY TUMOR-SUPPRESSOR GENES AND ONCOGENES

被引：83

作者：

CANMAN, CE

KASTAN, MB

机构：

[1] Johns Hopkins Oncology Center Oncology, Baltimore, MD 21287, 3-109

来源：

SEMINARS IN CANCER BIOLOGY | 1995年 / 6卷 / 01期

关键词：

APOPTOSIS; BCL-2; BCR-ABL; C-MYC; P53;

D O I：

10.1006/scbi.1995.0003

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：17 / 25

页数：9

共 90 条

[31] PARTICIPATION OF CYCLIN-A IN MYC-INDUCED APOPTOSIS [J].