Other highlights in the September 18 issue of JNCI

September 17, 2002

Smoking Associated with Increased Risk of Cervical Cancer Among Human Papillomavirus-Infected Women

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 findings appear in the September 18 issue of the Journal of the National Cancer Institute.

Malignant Urothelial Cells May be Susceptible to Apoptosis by CD40 Ligation

In epithelial cells, binding of the cell-surface receptor CD40 to its ligand, CD40L, can cause different effects, including apoptosis (cell death). Urszula Bugajska, Ph.D. and Ludwik Trejdosiewicz, Ph.D., of the Cancer Research U.K. Clinical Centre, St. James's University Hospital in Leeds, and their colleagues examined the effects of CD40 ligation on the survival of normal and malignant human urothelial cells that express CD40. They found that the apoptotic responses of the cells to CD40 ligation depended on how CD40L was presented to the cells, suggesting that susceptibility to CD40 ligation-induced apoptosis may be a useful therapeutic approach for eliminating malignant urothelial cells. They add that the loss of CD40 expression by urothelial cells may be important in the development and progression of bladder cancer. The findings appear in the September 18 issue of the Journal of the National Cancer Institute.
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Attribution to the Journal of the National Cancer Institute is requested in all news coverage.

Journal of the National Cancer Institute

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