Other highlights of the April 2 JNCI

April 01, 2003

Genetic Factors for Breast Density May Be Associated with Breast Cancer Risk

The genes that determine a woman's breast density may also determine her risk of breast cancer, according to a study in the April 2 issue of the Journal of the National Cancer Institute. Elad Ziv, M.D., of the UCSF Mount Zion Women's Health Clinical Research Center, and his colleagues found that, compared with women who had fatty breasts, women with denser breasts were more likely to have first-degree relatives with breast cancer. Their study involved an analysis of data from women who participated in the San Francisco Mammography Registry. "Our analysis is consistent with the possibility of there being a gene or genes that affect both breast density and the risk of breast cancer," the authors write. They note however, that genes that account for the association between breast density and breast cancer risk have yet to be identified.

Contact: Eve Harris, University of California San Francisco, 415-885-7277, eharris@pubaff.ucsf.edu.

Compound Slows Tumor Growth in Mice by Blocking Blood Supply

A compound called YC-1, developed for the treatment of circulation disorders, appears to slow tumor growth by blocking angiogenesis, or the formation of new blood vessels, according to study in the April 2 issue of the Journal of the National Cancer Institute. YC-1 may become the first anticancer agent to slow tumor growth by targeting HIF-1a, a transcription factor that enables cells to survive under low oxygen conditions. Eun-Jin Yeo and Jong-Wan Park, M.D., Ph.D., of Seoul National University College of Medicine, and colleagues show that human tumors in mice treated with YC-1 were smaller, had fewer blood vessels, and lower levels of the HIF-1a protein and of HIF-1 regulated genes than tumors from control-treated mice. The authors conclude that "YC-1 appears to halt tumor growth by blocking angiogenesis and not by a direct cytotoxic effect on tumor cells."

Genetic Instability Associated with Increased Risk of Bladder Cancer

Individuals with genetic instability, suggested by susceptibility to DNA damage, may be at increased risk of bladder cancer, according to a study in the April 2 issue of the Journal of the National Cancer Institute. Matthew B. Schabath, Xifeng Wu, M.D., Ph.D., and their colleagues at the University of Texas M. D. Anderson Cancer Center in Houston, used a technique called the comet assay to measure genetic instability by determining baseline and mutagen-induced DNA damage in the blood cells of 114 patients with bladder cancer and 145 healthy individuals. They found that patients with bladder cancer had higher levels of DNA damage than patients in the control group. The authors conclude that "genetic instability (both spontaneous and mutagen-induced) appears to be associated with the estimated relative risk of bladder cancer."

Contact: Laura Sussman, University of Texas M. D. Anderson Cancer Center, 713-792-0655, lsussman@mdanderson.org.

Vaccine Stimulates Antitumor Response in B-Cell Cancers

A new study shows that vaccination with lymphoma cells genetically altered to express high levels of costimulatory molecules (molecules involved in the activation of immune system T cells) stimulates an antitumor response in mice. The findings appear in the April 2 issue of the Journal of the National Cancer Institute. Javier Briones, M.D., Ronald Levy, M.D., of Stanford University School of Medicine, and their colleagues vaccinated mice with lymphoma cells that had been infected with either a recombinant virus encoding three costimulatory molecules or a control virus. The mice were injected with live lymphoma cells and mice vaccinated with cells infected with engineered virus survived longer than mice that received the control vaccine. Moreover, in mice with pre-existing lymphoma, tumor growth was slower in mice treated with the cells infected with engineered vaccine than in those vaccinated with the control vaccine. The authors say that their findings may open up new avenues for treating patients with B-cell lymphoma.

Contact: Amy Adams, Stanford University School of Medicine, 650-723-3900, amyadams@stanford.edu.
Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. 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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