March 2002

From Journal of the National Cancer Institute

Other highlights in the March 6 issue of JNCI

Tomato Products Associated With Decreased Prostate Cancer Risk
Frequent consumption of tomato products may be associated with a reduced risk of prostate cancer, concludes a study in the March 6 issue of the Journal of the National Cancer Institute.

Previous research has suggested that frequent consumption of tomato products or lycopene, an antioxidant in tomato sauce, may be associated with a lower risk of prostate cancer. To confirm these findings, Edward Giovannucci, M.D., Sc.D., and colleagues from Brigham and Women's Hospital and the Harvard School of Public Health analyzed tomato-product-consumption patterns and prostate cancer cases among roughly 47,400 men enrolled in the Health Professionals Follow-Up Study.

The researchers found that the consumption of tomato sauce was associated with a reduced risk of prostate cancer among men of Southern European descent (who typically have tomato-rich diets), and among men of Caucasian ancestry. The authors conclude that frequent consumption of tomato products is associated with a reduced risk of prostate cancer. They note, however, that it remains to be seen whether lycopene is the key compound in reducing prostate cancer risk.

Contact: Rob Hutchison, Brigham and Women's Hospital, (617) 534-1606; fax: (617) 534-1610; rhutchison@partners.org

Ras Gene May Play a Role in the Regression of Neuroblastomas
Neuroblastomas, tumors of the nervous system found almost exclusively in children, often regress spontaneously before showing any symptoms of disease. Previous studies have suggested that cell suicide may be responsible for this process. However, apoptosis, a well-known form of cell suicide, has not appeared to play a role.

In the March 6 issue of the Journal of the National Cancer Institute, Chifumi Kitanaka, M.D., Yoshiyuki Kuchino, Ph.D., of the National Cancer Center Research Institute in Tokyo, and their coworkers suggest another possible mechanism. They analyzed neuroblastoma tumor tissues and found that areas of tumor cell death contained increased expression of the Ras gene but lacked the characteristics of apoptosis. Cultured neuroblastoma cells injected with the Ras gene also showed signs of this so-called autophagic degeneration.

The authors conclude that Ras-mediated tumor cell death, rather than apoptosis, may play a key role in the spontaneous regression of neuroblastoma. They note that for cancer cells resistant to apoptosis, increasing the expression of the Ras gene may offer a new strategy for treatment of neuroblastomas.

Contact: Chifumi Kitanaka, National Cancer Center Research Institute, (81) 3-3542-2511; fax: (81) 3-3546-1369; ckitanak@ncc.go.jp

Growth Factor May be Involved in Some Head and Neck Cancers
The gastrin-releasing peptide (GRP) growth factor, which has been associated with tobacco-related lung injuries and lung cancers, may also be involved in some head and neck cancers, scientists report in the March 6 issue of the Journal of the National Cancer Institute.

Jennifer R. Grandis, M.D., and her colleagues from the University of Pittsburgh compared the expression of GRP and its receptor, GRPR, in 25 people with squamous cell carcinoma of the head and neck and 6 people without cancer. The researchers found a five-fold increase in the level of GRPR in the tissues of the people with cancer compared to people without cancer.

What's more, the researchers found increased levels of GRPR in healthy cells surrounding tumors, suggesting that increased levels of GRPR may be one of the first steps in the development of squamous cell head and neck cancer. The authors conclude that the regulatory pathway mediated by GRP and GRPR may be a target for new therapies for squamous cell carcinoma of the head and neck.

Contact: Clare Collins, University of Pittsburgh Medical Center, (412) 624-2607; fax: (412) 624-3184; collcx@msx.upmc.edu

Receptor Inactivation By Methylation May Be Associated with Prostate Cancer
Certain genes that code for steroid hormone receptors appear to be inactivated by methylation in prostate cancer tissue and cell lines, a new study suggests. The findings appear in the March 6 issue of the Journal of the National Cancer Institute.

Rajvir Dahiya, Ph.D., of the University of California, San Francisco, and his coworkers compared the presence of methylation of estrogen, androgen, and progesterone receptor genes in cancerous and normal prostate tissue from 38 people with prostate cancer and five prostate cancer cell lines.

The research team found that two forms of the estrogen receptor were methylated in all cell lines and almost all tissues. These receptors remained unmethylated in all normal tissues. The androgen receptor was also methylated in some cancerous tissues, but the progesterone receptor was unmethylated in all tissues. Demethylization of the receptors seemed to restore their activity. The researchers conclude that certain steroid hormone receptors may be inactivated by methylation in prostate cancer tissues and cell lines.

Contact: Eve Harris, University of California, San Francisco, (415) 885-7277; fax: (415) 502-1804; eharris@pubaff.ucsf.edu

Attribution to the Journal of the National Cancer Institute is requested in all news coverage.











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