Molecular epidemiology: Insights into cancer susceptibility, risk assessment, and prevention

被引:218
作者
Perera, FP
机构
[1] Columbia University, School of Public Health, Div. of Environ. Health Sciences, New York, NY 10032, 60 Haven Ave.
来源
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE | 1996年 / 88卷 / 08期
关键词
D O I
10.1093/jnci/88.8.496
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Recent molecular epidemiologic research provides compelling new evidence that environmental factors are major contributors to human cancer and that their risks are strongly influenced by genetic and acquired susceptibility. In particular, molecular epidemiology has demonstrated substantial variability in biologic response to carcinogens and suggests that certain groups-such as the very young, those with predisposing genetic traits or nutritional deficits, and even certain ethnic groups-are likely to have greater risk from selected exposures than other members of the population. This work implies that major gains in prevention of cancer, which will claim more than 554 000 American lives this year, will necessitate health and regulatory policies that protect these more susceptible groups and individuals from risks of man-made and naturally occurring environmental carcinogens. The specific implication from this research is that, to be effective in prevention, risk assessments developed in support of these policies by regulatory bodies, such as the Environmental Protection Agency, should reflect the available scientific data on individual variability in both exposure and susceptibility.
引用
收藏
页码:496 / 509
页数:14
相关论文
共 197 条
[11]  
BARTSCH H, 1992, HUMAN CANCER EPIDEMI, P189
[12]  
BEARDSLEY T, 1994, RISK POLICY REP 0315
[13]  
BEARDSLEY T, 1995, SCI AM 0628
[14]   GENETIC RISK AND CARCINOGEN EXPOSURE - A COMMON INHERITED DEFECT OF THE CARCINOGEN-METABOLISM GENE GLUTATHIONE-S-TRANSFERASE M1 (GSTM1) THAT INCREASES SUSCEPTIBILITY TO BLADDER-CANCER [J].
BELL, DA ;
TAYLOR, JA ;
PAULSON, DF ;
ROBERTSON, CN ;
MOHLER, JL ;
LUCIER, GW .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1993, 85 (14) :1159-1164
[15]   GENOTYPE-PHENOTYPE DISCORDANCE FOR HUMAN ARYLAMINE N-ACETYLTRANSFERASE (NAT2) REVEALS A NEW SLOW-ACETYLATOR ALLELE COMMON IN AFRICAN-AMERICANS [J].
BELL, DA ;
TAYLOR, JA ;
BUTLER, MA ;
STEPHENS, EA ;
WIEST, J ;
BRUBAKER, LH ;
KADLUBAR, FF ;
LUCIER, GW .
CARCINOGENESIS, 1993, 14 (08) :1689-1692
[16]  
Bennett William P., 1995, Proceedings of the American Association for Cancer Research Annual Meeting, V36, P699
[17]   DOES A GENOTOXIC CARCINOGEN CONTRIBUTE TO HUMAN BREAST-CANCER - THE VALUE OF MUTATIONAL SPECTRA IN UNRAVELING THE ETIOLOGY OF CANCER [J].
BIGGS, PJ ;
WARREN, W ;
VENITT, S ;
STRATTON, MR .
MUTAGENESIS, 1993, 8 (04) :275-283
[18]   MOLECULAR THEMES IN ONCOGENESIS [J].
BISHOP, JM .
CELL, 1991, 64 (02) :235-248
[19]   NOVEL PATTERN OF P53 GENE-MUTATIONS IN AN AMERICAN BLACK COHORT WITH HIGH MORTALITY FROM BREAST-CANCER [J].
BLASZYK, H ;
VAUGHN, CB ;
HARTMANN, A ;
MCGOVERN, RM ;
SCHROEDER, JJ ;
CUNNINGHAM, J ;
SCHAID, D ;
SOMMER, SS ;
KOVACH, JS .
LANCET, 1994, 343 (8907) :1195-1197
[20]   THE DATA SUPPORT A ROLE FOR ANTIOXIDANTS IN REDUCING CANCER RISK [J].
BLOCK, G .
NUTRITION REVIEWS, 1992, 50 (07) :207-213