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Original Summaries of Selected CANCERLIT Records
Cancer Prevention

Last modified on: Tuesday, April 20, 1999 10:52:30
Copyright © 1994-2008, Information Ventures, Inc.
Green tea has been shown to inhibit the occurrence of tumors in experimental animals, but human studies have been inconsistent. The problem may lie in a relative specificity for the cancer type against which the active components of tea provide protection. A study from the University of Minnesota in Minneapolis (ICDB/95609429), assessed the link between drinking non-herbal tea and cancer incidence by food questionnaire. This cohort study of 35,369 postmenopausal women in Iowa involved a seven-year follow-up period during which there were 2576 non-skin cancer cases. The scientists reported inverse associations between tea consumption and risk for cancers of the stomach, oropharynx, esophagus, and kidney. In stomach, esophageal and oral cancers, a total of 58 cases, risk ratios fell from 1.0, to 0.86, and 0.25 (p trend = 0.022) in going from non-tea-drinking and infrequent (less than weekly) to frequent (daily) tea intake. There was over a 50% lower risk of these cancers associated with daily tea consumption. The overall cancer risk was not affected, and neither were other cancers.

The relationship between cancer incidence and dietary constituents involves many factors that combine to produce a complicated pattern of interactions. Among these factors are the levels of critical enzymes in the body. One of these is glutathione-S-transferase which acts as a protective agent by combining pollutants and toxic substances with the sulfur-containing glutathione so that they are made innocuous. A study from the Harvard School of Public Health, Harvard Medical School and the Massachusetts General Hospital (ICDB/95609450), looked at these relationships in a hospital-based case-control study of 220 lung cancer cases and 274 controls. Deletion of the gene for glutathione-S-transferase (GSTM1) would be expected to increase the risk for lung cancer, and indeed there were increased odds ratios for GSTM1 loss, with an odds ratio 1.2, for all lung tumors combined, 1.8 for adenocarcinomas, and 1.2 small cell cancers. Vitamin C modified this effect for all tumors combined, but among specific histological types, this effect was only evident for small cell lung cancer, and not adenocarcinoma. Loss of GSTM1 increased the risk of small cell cancer about four- fold among subjects in the lowest tertile of vitamin C intake (odds ratio 3.8) but had no effect among those in the medium and high tertiles (odds ratios 1.5 and 0.5, respectively). There was also evidence of an effect of intake of vitamins E, D and B6.

October, 1995
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