News Release

Other highlights of the May 21 JNCI

Peer-Reviewed Publication

Journal of the National Cancer Institute

  • Selenium May Lower Risk of Esophageal Cancer in People with Barrett's Esophagus: Higher serum selenium levels appear to be associated with a reduced risk of progression toward esophageal cancer among people with Barrett's esophagus, according to a new study. Rebecca E. Rudolph, M.D., of the Fred Hutchinson Cancer Research Center, Seattle, and her colleagues examined 399 people with Barrett's esophagus and found that people with higher concentrations of selenium in their blood were less likely to have increased 4N fraction, aneuploidy, and high-grade dysplasia-three markers of cancer progression. These individuals also were less likely to have lost the portion of chromosome 17 that contains the p53 tumor suppressor gene. The authors suggest that "selenium might reduce cancer risk among persons with Barrett's esophagus by preventing the inactivation of p53 or by preventing further neoplastic progression after p53 has been inactivated."

    Contact: Kristen Woodward, Fred Hutchinson Cancer Research Center, 206-667-5095; kwoodwar@fhcrc.org.

  • Cyclin D1 May be Involved in Ovarian Cancer Growth: Researchers have found a second mechanism through which lysophosphatidic acid (LPA) may promote ovarian tumor growth. Yu-Long Hu, Ph.D., and Robert Jaffe, M.D., of the University of California, San Francisco, and their colleagues found that LPA treatment increases cyclin D1 protein levels in ovarian cancer cells but not in normal ovarian cells. Cyclin D1 is a key cell cycle regulator that is overexpressed in various human cancers, including ovarian cancer. A previous study found that LPA can stimulate ovarian cancer growth by increasing the expression of vascular endothelial growth factor (VEGF), which promotes angiogenesis (the formation of new blood vessels). The new findings suggest that LPA stimulates ovarian tumor growth through dual mechanisms. Finding ways to block these pathways may lead to new therapies for ovarian cancer, the authors say.

    Contact: Jennifer O'Brien, University of California, San Francisco, 415-476-2557 jobrien@pubaff.ucsf.edu.

  • Discovery May Lead to Less Toxic Cancer Immunotherapy: Researchers have identified a region of cytokine interleukin-2 (IL-2) that may be responsible for causing vasopermeability (i.e., capillary leakage), a side effect that limits use of the drug as a cancer immunotherapy. Alan Epstein, M.D., Ph.D., of the University of Southern California, Keck School of Medicine, and his colleagues synthesized peptide fragments of IL-2, linking them to tumor-targeting antibodies, and examining their ability to induce tumor vascular permeability. One fragment, permeability-enhancing peptide (PEP), had the same vasopermeability activity as IL-2 but lacked cytokine activity, suggesting that the vasopermeability and cytokine activities of IL-2 can be separated. The authors say that the identification of PEP should help researchers find ways to decrease the toxicity of IL-2.

    Contact: Jon Weiner, University of Southern California, Keck School of Medicine, 323-442-2830, jonweine@usc.edu.

  • Cell Growth Inhibitor May be Involved in Melanoma Susceptibility: A new study suggests that the p16 growth inhibitor may play a role in susceptibility to melanoma, the malignant form of skin cancer. Elena V. Sviderskaya, Ph.D., and Dorothy C. Bennett, Ph.D., of the St. George's Hospital Medical School in London, United Kingdom, and their colleagues examined melanocytes (pigment producing cells) taken from two patients with melanoma who had inactivated p16 alleles. They found that these melanocytes proliferated longer than normal melanocytes, suggesting that inactivation of p16 resulted in the impairment of cell growth inhibitory mechanisms. The authors say that their findings may provide some basis for the role of p16 in susceptibility to melanoma.

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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.


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