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TP53 Mutation Spectrum in Lung Cancer Is Not Different in Women and Men

¹ Laboratory of Carcinogenesis and Biomarkers, Clinical Breast Care Project Immunology and Research Center, Uniformed Services University of Health Sciences; ² Laboratory of Human Carcinogenesis, National Cancer Institute, Center for Cancer Research, Bethesda, Maryland; and ³ Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, District of Columbia

Requests for reprints: Curtis C. Harris, Laboratory of Human Carcinogenesis, National Cancer Institute, Room 3068, Building 37, 37 Convent Drive, Bethesda, MD 20892-4255. Phone: 301-496-2048; Fax: 301-496-0497. E-mail: Curtis_Harris{at}nih.gov

Whether women are more susceptible to lung cancer than men has been controversial. Several case-control studies suggested that women have greater risk of lung cancer compared with men at similar levels of cigarette smoking, whereas some large cohort studies failed to observe this association. Other studies indicated that lung cancer may have biological characteristics and mechanisms of carcinogenesis that are gender specific. Therefore, we hypothesized that women are more susceptible to the carcinogenic effects of tobacco smoke exposure, as evidenced by a higher frequency of G:C-to-T:A somatic mutations in tumors from women in comparison with men at similar levels of tobacco smoke exposure. To investigate our hypothesis, we examined the TP53 mutational spectrum in a case-only (102 women and 201 men) series study where complete smoking information was available. A similar frequency and type of somatic TP53 mutations were observed in women and men. In conclusion, our study indicates that the TP53 mutation spectrum is similar in women and men. Our results are consistent with a recent large cohort study and summary of previous cohort studies, suggesting that women likely have equivalent susceptibility to lung cancer as men.

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