Volume 88, Issue 5 p. 885-898
Prospect

Apoptosis and lung cancer: A review

Narayan Shivapurkar

Narayan Shivapurkar

Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593

Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593

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Jyotsna Reddy

Jyotsna Reddy

Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593

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Preet M. Chaudhary

Preet M. Chaudhary

Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593

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Adi F. Gazdar

Corresponding Author

Adi F. Gazdar

Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593

Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593

Hamon Center for Therapeutic Oncology Research, NB8. 106, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX, 75390-8593.Search for more papers by this author
First published: 26 February 2003
Citations: 154

Abstract

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. J. Cell. Biochem. 88: 885–898, 2003. © 2003 Wiley-Liss, Inc.

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