A new study shows that common mutations in genes that regulate estrogen metabolism are not associated with breast cancer risk.
Several studies have suggested that circulating levels of sex hormones, particularly estrogen, are associated with breast cancer risk, but it is not clear whether changes in the genes that control these levels are associated with breast cancer risk.
Alison M. Dunning, Ph.D., of Cancer Research UK in Cambridge, England, and colleagues looked at common variations, called single nucleotide polymorphisms or SNPs, in genes that regulate estrogen metabolism. They found SNPs in two genes that affected estrogen metabolism. However, there was no association between the common variations in the genes and breast cancer risk.
Contact: Michael Regnier, Cancer Research UK, 44-207-061-8302, michael.regnier@cancer.org.uk
Study Suggests a Possible Target for Treatment of Gastric Cancer
Inhibition of hypoxia-inducible factor 1alpha (HIF-1alpha) activity reduces angiogenesis, vessel maturation, and tumor growth in gastric cancer cells, according to a new study. The authors suggest that HIF-1alpha may be a target for future gastric cancer treatments.
HIF-1 controls expression of vascular endothelial growth factor (VEGF), which contributes to tumor angiogenesis. Overexpression of HIF-1alpha, a subunit of HIF-1, is associated with tumor angiogenesis and tumor cell proliferation. Lee M. Ellis, M.D., of the University of Texas M. D. Anderson Cancer Center in Houston, and colleagues examined the effects of inhibiting HIF-1alpha on VEGF expression and angiogenesis and tumor growth in human gastric cancer.
They found that inhibition of HIF-1alpha activity decreased angiogenesis and the growth of human gastric cancer cells, which suggests that HIF-1alpha could be a valid target for the treatment of gastric cancer.
Contact: Laura Sussman, Communications Office, M. D. Anderson Cancer Center, 713-745-2457, lsussman@mdanderson.org
Study Elucidates Molecular Interactions of Bone Sialoprotein in Cancer Cell Invasion
Although bone sialoprotein (BSP) is overexpressed in many malignant tissues, including breast, lung, prostate, and thyroid cancers, its role in tumor progression has remained unknown. In a new study, Abdullah Karadag, M.D., Ph.D., of the National Institute of Dental and Craniofacial Research in Bethesda, Md., and colleagues looked into whether BSP's interaction with other molecules enhances the invasiveness of cancer cells. They found that when BSP and two other molecules--matrix metalloproteinase 2 and integrin alphavbeta3--form a cell-surface trimolecular complex, cancer cells appear to become more invasive.
Contact: Robert Kuska, National Institute of Dental and Craniofacial Research, 301-594-7560, kuskar@mail.nih.gov
Also in the June 16 JNCI:
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. Visit the Journal online at http://jncicancerspectrum.oupjournals.org/.
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JNCI Journal of the National Cancer Institute