Current and past smoking may increase the risk of cervical cancer among women who have been infected with the human papillomavirus (HPV), according to a study in the September 18 issue of the Journal of the National Cancer Institute.
Philip E. Castle, Ph.D., of the National Cancer Institute, and his colleagues looked at the association between various risk factors and cervical cancer among 1,812 women who had tested positive for oncogenic HPV DNA. Oral contraceptive use and history of live births were not associated with the risk of cervical cancer or its precursor, cervical intraepithelial neoplasia grade 3 (CIN3). However, former and current smokers appeared to have an increased risk of cervical cancer and CIN3 compared with women who never smoked.
The authors say that future studies should examine whether biomarkers associated with smoking, such as DNA damage, are present in cervical tissue and whether such biomarkers can be detected before the development of CIN3 or cervical cancer.
Majority of Ovarian Tumors With BRCA2 Mutations Also Have BRCA1 Mutations
Mutations in the BRCA1 and BRCA2 tumor suppressor genes have been shown to play a role in hereditary ovarian cancer. To explore the interactions of mutations in these genes in ovarian cancer, Jeffrey L. Hilton, M.D., and Richard E. Buller, M.D., Ph.D., of the University of Iowa Hospitals and Clinics, and their colleagues looked for BRCA2 mutations in ovarian tumors previously screened for BRCA1 mutations. They found that multiple genetic mechanisms are responsible for the inactivation of BRCA2 in these tumors and that a majority of the tumors with BRCA2 dysfunciton also had BRCA1 dysfunction. The authors conclude that "some degree of BRCA1 and/or BRCA2 dysfunction may be of nearly universal importance for the process of ovarian carcinogenesis." The findin
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Contact: Linda Wang
jncimedia@oupjournals.org
301-841-1287
Journal of the National Cancer Institute
17-Sep-2002