© 2004 by Oxford University Press
© 2004 Oxford University Press
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In Brief
Study Finds Most Antioxidant Supplements Provide No Protection Against Gastrointestinal Cancers
A review of clinical trials that tested the effects of antioxidant supplements on the risk of gastrointestinal cancers found that the antioxidants, alone and in combination, were not effective in reducing cancer risk.
In the October 2 issue of The Lancet, Goran Bjelakovic, M.D., of the University of Nis in Serbia and Montenegro, and colleagues reviewed 14 randomized trials that had compared antioxidant supplements with placebo for the prevention of gastrointestinal cancers. Overall, there was no association between supplementation with beta-carotene; vitamins A, C, or E; and selenium, alone or in combination, and decreased risk of colorectal, esophageal, gastric, liver, or pancreatic cancers.
In the trials categorized as high quality, there was a small increased risk in mortality associated with taking antioxidant supplements. This risk was greatest for the combination of beta-carotene and vitamin A and for beta-carotene and vitamin E.
Safety Warning Issued on Drugs for Metastatic Bone Disease
Novartis and the U.S. Food and Drug Administration have issued a safety warning on Aredia (pamindronate disodium) injection and Zometa (zoledronic acid) injection after cases of osteonecrosis, or bone deterioration, of the jaw were reported in cancer patients being treated with the drugs.
Most of the cases of osteonecrosis were associated with dental procedures, such as tooth extraction, and patients who are taking these drugs are advised to avoid invasive dental procedures. There are no data to suggest whether or not the risk of osteonecrosis of the jaw decreases if patients stop taking the drugs.
The safety warning, including a letter from Novartis Oncology, is available online from the FDA at http://www.fda.gov/medwatch/SAFETY/2004/safety04.htm#zometa.
Two Trials Suggest Docetaxel Improves Survival in Metastatic Prostate Cancer
Two new studies have found that treatment regimens for metastatic, hormone-refractory prostate cancer that include docetaxel are associated with better survival than mitoxantrone-based regimens.
In the first study, Ian F. Tannock, M.D., Ph.D., of Princess Margaret Hospital in Toronto, and colleagues randomly assigned 1,006 men with metastatic hormone-refractory prostate cancer to receive either mitoxantrone every 3 weeks, docetaxel every 3 weeks, or docetaxel weekly for 5 of every 6 weeks. All men received prednisone twice daily. The men who received docetaxel every 3 weeks had higher median overall survival compared with those in the mitoxantrone group, but the weekly docetaxel group had similar survival to that of the mitoxantrone group.
In a second study, Daniel P. Petrylak, M.D., and colleagues in the Southwest Oncology Group randomly assigned 770 men with metastatic, hormone-independent prostate cancer to receive docetaxel plus estramustine or mitoxantrone plus prednisone. Overall survival was longer in the docetaxel group (17.5 months) compared with the mitoxantrone group (15.6 months). However, grade 3 or 4 toxic effects were more common in the docetaxel group, and pain relief was similar in both groups.
The studies were published in the October 7 issue of the New England Journal of Medicine.
Oncogene Inactivation Prompts Tumor Regression in Mice
A new study has found that suppression of the MYC oncogene prompts regression of invasive liver cancers in a mouse model.
Dean W. Felsher, of Stanford University, and colleagues bred transgenic mice that overexpressed the MYC oncogene, which is one of the most commonly activated oncogenes in liver tumors. Mice that were continuously treated with doxycycline to suppress MYC expression remained disease free; mice taken off doxycycline—thereby activating MYC—succumbed to liver tumors within an average of 12 weeks.
When mice that developed liver tumors were later treated with doxycycline to suppress MYC, the mice experienced rapid and sustained tumor regression. Most of these cells eventually underwent cell death. However, some of the tumor cells differentiated back into various types of healthy liver cells.
The authors conclude that this differentiation capability may mean that MYC overexpression results in the malignant expansion of immature liver cells that resemble stem cells.
"[T]here are circumstances when the abatement of oncogene activation is sufficient to resume a normal physiological program even in cancer cells," the authors wrote in the October 10 advance online issue of Nature. "Our model system will provide a strategy to interrogate generally how oncogene inactivation uncovers the pluripotent differentiation of cancers and specifically identify the putative liver cancer stem cell."
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  D. Errante, N. Mannucci, D. Bernardi, A. Bianco, and L. Salvagno Comment on 'Jaw avascular bone necrosis associated with long-term use of biphosphonates' Ann. Onc., February 1, 2006; 17(2): 350 - 352. [Full Text] [PDF]
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