Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 88, Issue 5, Pages 885-898Publisher
WILEY
DOI: 10.1002/jcb.10440
Keywords
chemosensitivity; p53; lung cancer; apoptosis
Categories
Funding
- NCI NIH HHS [P50-CA70907] Funding Source: Medline
- NIAID NIH HHS [AI/AR47230] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available