THE CYP1A1 GENE AND CANCER SUSCEPTIBILITY

被引：225

作者：

KAWAJIRI, K ^{[1
]}

NAKACHI, K ^{[1
]}

IMAI, K ^{[1
]}

WATANABE, J ^{[1
]}

HAYASHI, S ^{[1
]}

机构：

[1] SAITAMA CANC CTR,RES INST,DEPT EPIDEMIOL,INA,SAITAMA 362,JAPAN

来源：

CRITICAL REVIEWS IN ONCOLOGY/HEMATOLOGY | 1993年 / 14卷 / 01期

关键词：

D O I：

10.1016/1040-8428(93)90007-Q

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

A close correlation between cigarette smoking associated lung cancer incidence and an Msp I restriction fragment length polymorphism (RFLP) of the human P-450 1A1 (CYP1A1) gene was found in a Japanese population in terms of genotype frequency and cigarette dose. A Val/Ile codon difference in the primary structure of the CYP1A1 protein (Val-, Ile-type) was in linkage disequilibrium with the Msp I RFLP. A synergistic increase in susceptibility to lung cancer was found when combining genotyping of CYP1A1 and the Mu-class of glutathione S-transferase (GST1). Interindividual variability in the genetic make-up of carcinogen metabolizing enzymes may thus be a key host factor to explain the differences in susceptibility to chemical carcinogenesis among individuals. © 1993.

引用

页码：77 / 87

页数：11

共 91 条

[1] SMOKING AND PERIPHERAL TYPE OF CANCER ARE RELATED TO HIGH-LEVELS OF PULMONARY CYTOCHROME-P450IA IN LUNG-CANCER PATIENTS [J].

ANTTILA, S ;

HIETANEN, E ;

VAINIO, H ;

CAMUS, AM ;

GELBOIN, HV ;

PARK, SS ;

HEIKKILA, L ;

KARJALAINEN, A ;

BARTSCH, H .

INTERNATIONAL JOURNAL OF CANCER, 1991, 47 (05) :681-685

[2] METABOLIC OXIDATION PHENOTYPES AS MARKERS FOR SUSCEPTIBILITY TO LUNG-CANCER [J].

AYESH, R ;

IDLE, JR ;

RITCHIE, JC ;

CROTHERS, MJ ;

HETZEL, MR .

NATURE, 1984, 312 (5990) :169-170

[3]

BALE AE, 1987, CYTOGENET CELL GENET, V46, P574

[4] CLONING OF THE AH-RECEPTOR CDNA REVEALS A DISTINCTIVE LIGAND-ACTIVATED TRANSCRIPTION FACTOR [J].

BURBACH, KM ;

POLAND, A ;

BRADFIELD, CA .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (17) :8185-8189

[5] HUMAN CYTOCHROME P-450PA (P-450IA2), THE PHENACETIN O-DEETHYLASE, IS PRIMARILY RESPONSIBLE FOR THE HEPATIC 3-DEMETHYLATION OF CAFFEINE AND N-OXIDATION OF CARCINOGENIC ARYLAMINES - (AROMATIC-AMINES HETEROCYCLIC AMINES CARCINOGEN METABOLISM) [J].

BUTLER, MA ;

IWASAKI, M ;

GUENGERICH, FP ;

KADLUBAR, FF .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (20) :7696-7700

[6] RELEVANCE OF METABOLIC POLYMORPHISMS TO HUMAN CARCINOGENESIS - EVALUATION OF EPIDEMIOLOGIC EVIDENCE [J].

CAPORASO, N ;

LANDI, MT ;

VINEIS, P .

PHARMACOGENETICS, 1991, 1 (01) :4-19

[7] LUNG-CANCER AND THE DEBRISOQUINE METABOLIC PHENOTYPE [J].

CAPORASO, NE ;

TUCKER, MA ;

HOOVER, RN ;

HAYES, RB ;

PICKLE, LW ;

ISSAQ, HJ ;

MUSCHIK, GM ;

GREENGALLO, L ;

BUIVYS, D ;

AISNER, S ;

RESAU, JH ;

TRUMP, BF ;

TOLLERUD, D ;

WESTON, A ;

HARRIS, CC .

JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1990, 82 (15) :1264-1272

[8] GST1 GENE DELETION DETERMINED BY POLYMERASE CHAIN-REACTION [J].

COMSTOCK, KE ;

SANDERSON, BJS ;

CLAFLIN, G ;

HENNER, WD .

NUCLEIC ACIDS RESEARCH, 1990, 18 (12) :3670-3670

[9] INDUCTION OF MICROSOMAL CYTOCHROME-P-450 ENZYMES - THE 1ST BRODIE,BERNARD,B. LECTURE AT PENNSYLVANIA-STATE-UNIVERSITY [J].

CONNEY, AH .

LIFE SCIENCES, 1986, 39 (26) :2493-2518

[10]

CRESPI CL, 1991, CARCINOGENESIS, V12, P197

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