TY - JOUR
T1 - Oral cancer prevention
T2 - The case for carotenoids and anti-oxidant nutrients
AU - Garewal, Harinder
AU - Meyskens, Frank
AU - Friedman, Sherry
AU - Alberts, David
AU - Ramsey, Lois
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1993/9
Y1 - 1993/9
N2 - The most convincing evidence for a preventive role for any modality is obviously demonstration of incidence reduction produced by that modality. However, cancer prevention trials with cancer incidence as an endpoint have logistic problems rendering them essentially impossible to conduct for most malignancies. Hence a workable strategy often involves analysis of other, indirect lines of evidence to reach conclusions. For oral cancer, epidemiologic evidence points to a protective role for foods rich in carotenoids. Other dietary anti-oxidents, such as Vitamin C, are also implicated. Similarly, laboratory evidence points to a carcinogenesis inhibitory role for both retinoids and carotenoids. Clinical studies have targeted premalignant lesions, i.e., oral leukoplakia. For orver two decades the efficiency of retinoids, natural and synthetic, has been known. Nevertheless, it has been difficult to translate this into a recommendation for prevention because of the toxicity of retinoids. The synthetic retinoid most often used in these trials is 13-cis-retinoic acid. This compound is toxic even at very low doses (0.1 mg/kg/day), particularly when given over several weeks to months. Hence, although effective, it cannot be advocated for prevention of oral cavity cancer. Studies with nontoxic antioxidents, such as β-carotene, are much more recent. Early results are promising in that β-carotene, alone or in combination with other nutrients, can reverse oral leukoplakia without toxicity in the short-term trials. Studies currently under way will demonstrate whether durable remissions can be obtained using this strategy. It should be emphasized that such long-term trials are problematic to conduct with the toxic retinoids because the risks of prolonged exposure to them outweighs the chance of cancer development in the usual leukoplakia lesion.
AB - The most convincing evidence for a preventive role for any modality is obviously demonstration of incidence reduction produced by that modality. However, cancer prevention trials with cancer incidence as an endpoint have logistic problems rendering them essentially impossible to conduct for most malignancies. Hence a workable strategy often involves analysis of other, indirect lines of evidence to reach conclusions. For oral cancer, epidemiologic evidence points to a protective role for foods rich in carotenoids. Other dietary anti-oxidents, such as Vitamin C, are also implicated. Similarly, laboratory evidence points to a carcinogenesis inhibitory role for both retinoids and carotenoids. Clinical studies have targeted premalignant lesions, i.e., oral leukoplakia. For orver two decades the efficiency of retinoids, natural and synthetic, has been known. Nevertheless, it has been difficult to translate this into a recommendation for prevention because of the toxicity of retinoids. The synthetic retinoid most often used in these trials is 13-cis-retinoic acid. This compound is toxic even at very low doses (0.1 mg/kg/day), particularly when given over several weeks to months. Hence, although effective, it cannot be advocated for prevention of oral cavity cancer. Studies with nontoxic antioxidents, such as β-carotene, are much more recent. Early results are promising in that β-carotene, alone or in combination with other nutrients, can reverse oral leukoplakia without toxicity in the short-term trials. Studies currently under way will demonstrate whether durable remissions can be obtained using this strategy. It should be emphasized that such long-term trials are problematic to conduct with the toxic retinoids because the risks of prolonged exposure to them outweighs the chance of cancer development in the usual leukoplakia lesion.
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U2 - 10.1006/pmed.1993.1064
DO - 10.1006/pmed.1993.1064
M3 - Article
C2 - 8234210
AN - SCOPUS:0027445513
VL - 22
SP - 701
EP - 711
JO - Preventive Medicine
JF - Preventive Medicine
SN - 0091-7435
IS - 5
ER -