Apoptosis and lung cancer: A review

被引:212
作者
Shivapurkar, N
Reddy, J
Chaudhary, PM
Gazdar, AF
机构
[1] Univ Texas, SW Med Ctr, Hamon Ctr Therapeut Oncol Res, Dallas, TX 75390 USA
[2] Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75390 USA
[3] Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75390 USA
关键词
chemosensitivity; p53; lung cancer; apoptosis;
D O I
10.1002/jcb.10440
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
It is important to understand the molecular events that contribute to drug-induced apoptosis, and how tumors evade apoptotic death. Defects in apoptosis are implicated in both tumorigenesis and drug resistance, and these defects are cause of chemotherapy failures. These studies should explain the relationship between cancer genetics and treatment sensitivity, and should enable a more rational approach to anticancer drug design and therapy. Lung cancer is a major cause of cancer deaths throughout the world. Small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC) represent the two major categories of lung cancer that differ in their sensitivity to undergo apoptosis. The role of apoptosis regulation in lung cancer with major focus on the differential sensitivities of the major subtypes is reviewed. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:885 / 898
页数:14
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