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Other highlights in JNCI, June 12

Journal of the National Cancer Institute

AIDS-Related Cancers Decline with Introduction of Intense Antiretroviral Therapy

Higher immune cell counts in AIDS patients treated with highly active antiretroviral therapy (HAART) are associated a lower incidence of Kaposi sarcoma and non-Hodgkin lymphoma.

AIDS patients are at high risk for Kaposi sarcoma, non-Hodgkin lymphoma, and cervical cancer, but recent studies have found the incidence of Kaposi sarcoma and non-Hodgkin lymphoma has been declining in people with AIDS since the introduction of HAART in 1996. This therapy usually increases the number of patients' CD4 cells, also known as helper T-cells, and reduces the risks associated with infectious diseases.

Robert J. Biggar, M.D., of the National Cancer Institute in Bethesda, Md., and colleagues assessed the relationship between cancer incidence and patients' CD4 cell counts at the time of AIDS diagnosis by comparing cancer incidence in AIDS patients before and after HAART became available.

After 1996, the incidence of Kaposi sarcoma and non-Hodgkin lymphoma in AIDS patients decreased, while cervical cancer rates in AIDS patients increased. CD4 count was strongly associated with a decrease in Kaposi sarcoma and non-Hodgkin lymphoma rates, but not with cervical cancer rates.

"Our results illustrate the variable impact of immunity on the risk of AIDS-associated cancers with the range of CD4 counts in persons with AIDS," the authors write.

Contact: National Cancer Institute Press Office, 301-496-6641,

Oncogene Overexpression Is Associated with Aggressive Glioma

Researchers have determined that the cell cycle-related kinase gene (CCRK) may be involved in the development of glioblastoma multiforme, the most aggressive form of a type of brain tumor called glioma.

The median survival for patients with glioblastoma multiforme 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,

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 non-small-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. Additionally, deguelin reduced tumor growth in mice without any detectable toxic side effects.

"Extensive and complete chronic toxicity testing in clinical trials is warranted before the further development of deguelin as an anticancer therapeutic agent," the authors write.

Contact: Laura Sussman, press office, M. D. Anderson Cancer Center, 713-745-2457,

Also in the June 12 JNCI:


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