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Other highlights in JNCI, June 12

e is 12 to 15 months. Researchers hope that identifying the genes that control the progression of the disease will help them develop new therapies.

Samuel Ng, Ph.D., of the University of Hong Kong and colleagues analyzed the gene expression of CCRK in human glioma cell lines, in samples from glioma patients and normal brain tissue, and in mouse models.

They found that the overexpression of the CCRK gene was associated with a greater risk of developing glioma and increased tumor growth, whereas suppression of the gene was associated with the inhibition of tumor growth.

Our results support the rationale for developing CCRK as a potential therapeutic and diagnostic target for glioblastoma multiforme, and, possibly, other cancers, the authors write.

Contact: Marie Lin, University of Hong Kong, +852-22990776, mcllin@hkusua.hku.hk


Antitumor Compound Blocks Heat Shock Protein

Deguelin, a natural compound known to have antitumor properties, appears to disrupt the function of heat shock protein 90 (Hsp90), which cancer cells may need to grow.

Heat shock proteins are expressed in response to higher temperatures and help prevent disruptions in protein folding. Hsp90, in particular, is often overexpressed in cancer cells and maintains stability and function of several oncoproteins, known as client proteins.

Seung Hyun Oh, Ph.D., D.V.M., of the University of Texas M. D. Anderson Cancer Center in Houston, and colleagues investigated whether deguelin inhibits the function of Hsp90. Mice with transplanted human nonsmall-cell lung cancer, head and neck cancer, stomach cancer, or prostate cancer were treated with deguelin or placebo twice a day for 15-28 days.

The researchers showed that deguelin directly binds to Hsp90 and inhibits its functional activity, which results in a reduction in the expression of its client proteins. Ad
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Contact: Liz Savage
jncimedia@oxfordjournals.org
301-841-1287
Journal of the National Cancer Institute
12-Jun-2007


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