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Role of P63 Amplification and Overexpression in Lung Cancer Development*

Pierre P. Massion, MD; Peter M. Taflan, BS; S.M. Jamshedur Rahman, PhD; Pinar Yildiz, MD; Yu Shyr; David P. Carbone, MD; Adriana L. Gonzalez
Author and Funding Information

*From the Division of Allergy, Pulmonary and Critical Care Medicine (Drs. Massion, Yildiz, and Rahman, and Mr. Taflan); Department of Biostatistics (Mr. Shyr); Department of Medicine (Dr. Carbone); and the Vanderbilt Ingram Comprehensive Cancer Center (Ms. Gonzalez), Nashville, TN.

Correspondence to: Pierre P. Massion, MD, Vanderbilt Ingram Comprehensive Cancer Center, 2200 Pierce Ave, Preston Research Bldg 640, Nashville, TN 37232-6838.



Chest. 2004;125(5_suppl):102S. doi:10.1378/chest.125.5_suppl.102S-a
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The fight against lung cancer is greatly compromised by the lack of effective early detection strategies. Genomic abnormalities, and specifically the amplification of chromosomal region 3q26–3qter, in lung cancer represent a major signature of neoplastic transformation. Here, we address the significance of p53 homolog p63 mapping to 3q27 in lung tumorigenesis.

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