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DNA Damage and Repair Capacity in Patients With Lung Cancer: Prediction of Multiple Primary Tumors

Irene Orlow, Bernard J. Park, Urvi Mujumdar, Himali Patel, Puiki Siu-Lau, Brian A. Clas, Robert Downey, Raja Flores, Manjit Bains, Nabil Rizk, Gemma Dominguez, Jen Jani, Marianne Berwick, Colin B. Begg, Mark G. Kris, Valerie W. Rusch

From the Departments of Epidemiology and Biostatistics, Surgery, and Oncology, Memorial Sloan-Kettering Cancer Center, New York, NY; and the University of New Mexico, Albuquerque, NM

Corresponding author: Irene Orlow, PhD, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, Box 353, New York, NY 10021; e-mail: orlowi{at}mskcc.org

Purpose Patients who survive one occurrence of non–small-cell lung cancer (NSCLC) are at higher risk of a second malignancy. Capacity to repair damaged DNA may modulate individual susceptibility to develop lung cancer. Therefore, we evaluated constitutive and induced DNA damage, and repair capacity, in patients with multiple NSCLCs (cases) and compared the results to those obtained in patients with a single NSCLC (controls).

Patients and Methods One hundred eight cases and 99 controls matched by age, sex, and time since diagnosis were studied. DNA damage was assessed on peripheral blood lymphocytes by the comet assay before and after exposing cells to a tobacco-derived carcinogen, using the tail moment and the tail intensity as measures to assess baseline damage, induced damage and repair capacity.

Results Constitutive DNA damage, benzo(a)pyrene diol epoxide–induced damage, and repair after BPDE-induced damage were all significantly higher in cases than in controls. These results were confirmed in regression analyses adjusted for potential confounders.

Conclusion DNA damage as measured by the comet assay is associated with the development of multiple primary tumors in individuals with NSCLC.

Supported by the Society of Memorial Sloan-Kettering Cancer Center through their annual appeal and Steps for Breath.

Presented in part at the 41st Annual Meeting of the American Society of Clinical Oncology, Orlando FL, May 13-17, 2005; and at the 11th World Lung Cancer Meeting, Barcelona, Spain, July 3-6, 2005.

Authors’ disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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