DETERMINATION OF THE ALLELIC FREQUENCIES OF AN L-MYC AND A P53 POLYMORPHISM IN HUMAN LUNG-CANCER

被引:90
作者
WESTON, A
LINGCAWLEY, HM
CAPORASO, NE
BOWMAN, ED
HOOVER, RN
TRUMP, BF
HARRIS, CC
机构
[1] NCI, HUMAN CARCINOGENESIS LAB, BETHESDA, MD 20892 USA
[2] NCI, GENET EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA
[3] NCI, ENVIRONM EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA
[4] UNIV MARYLAND, SCH MED, DEPT PATHOL, BALTIMORE, MD 21201 USA
关键词
D O I
10.1093/carcin/15.4.583
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The L-myc and p53 genes have been implicated in lung cancer. Both of these genes have restriction fragment length polymorphisms (RFLPs) that could account for differential expression or activity of variant forms. An EcoRI restriction site in the L-myc gene was previously reported to be a predictor of poor prognosis in Japanese lung cancer patients. There are several RFLPs in the p53 gene. In exon 4 there is a polymorphism that codes for either an arginine or proline residue at codon 72. We previously reported the frequency of DNA-RFLPs at these gene loci revealed by EcoRI and AccII respectively. Here we report results from a study comparing lung cancer cases (n = 31) with chronic obstructive pulmonary disease controls (n = 49). No association was found between these RFLPs and disease status. Previous observations that the frequencies of these RFLPs varied by race were confirmed. The p53 arginine allele was found to be more common in Caucasians (0.71) than African-Americans (0.50). The EcoRI restriction site present allele in L-myc was more frequent in African-Americans (0.71) than Caucasians (0.49). Thus, the allelic frequency for L-myc was similar in African-Americans to that reported for Japanese, and the allelic frequency for p53 was similar in Caucasians to that reported for Japanese.
引用
收藏
页码:583 / 587
页数:5
相关论文
共 41 条
  • [1] [Anonymous], 1988, MAPPING OUR GENES GE
  • [2] CODON-72 POLYMORPHISM OF THE TP53 GENE
    ARA, S
    LEE, PSY
    HANSEN, MF
    SAYA, H
    [J]. NUCLEIC ACIDS RESEARCH, 1990, 18 (16) : 4961 - 4961
  • [3] GENETIC MONITORING OF HUMAN POLYMORPHIC CANCER SUSCEPTIBILITY GENES BY POLYMERASE CHAIN-REACTION - APPLICATION TO GLUTATHIONE TRANSFERASE MU
    BELL, DA
    THOMPSON, CL
    TAYLOR, J
    MILLER, CR
    PERERA, F
    HSIEH, LL
    LUCIER, GW
    [J]. ENVIRONMENTAL HEALTH PERSPECTIVES, 1992, 98 : 113 - 117
  • [4] A MURINE MACROPHAGE CELL-LINE, IMMORTALIZED BY V-RAF AND V-MYC ONCOGENES, EXHIBITS NORMAL MACROPHAGE FUNCTIONS
    BLASI, E
    RADZIOCH, D
    DURUM, SK
    VARESIO, L
    [J]. EUROPEAN JOURNAL OF IMMUNOLOGY, 1987, 17 (10) : 1491 - 1498
  • [5] BOTSTEIN D, 1980, AM J HUM GENET, V32, P314
  • [6] Caporaso N. E., 1992, Environmental Health Perspectives, V98, P101, DOI 10.2307/3431254
  • [7] LUNG-CANCER AND THE DEBRISOQUINE METABOLIC PHENOTYPE
    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
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1990, 82 (15) : 1264 - 1272
  • [8] RECESSIVE MUTANT-GENES PREDISPOSING TO HUMAN CANCER
    CAVENEE, WK
    KOUFOS, A
    HANSEN, MF
    [J]. MUTATION RESEARCH, 1986, 168 (01): : 3 - 14
  • [9] DELACALLEMARTIN O, 1990, NUCLEIC ACIDS RES, V18, P4963, DOI 10.1093/nar/18.16.4963
  • [10] A GENETIC-LINKAGE MAP OF THE HUMAN GENOME
    DONISKELLER, H
    GREEN, P
    HELMS, C
    CARTINHOUR, S
    WEIFFENBACH, B
    STEPHENS, K
    KEITH, TP
    BOWDEN, DW
    SMITH, DR
    LANDER, ES
    BOTSTEIN, D
    AKOTS, G
    REDIKER, KS
    GRAVIUS, T
    BROWN, VA
    RISING, MB
    PARKER, C
    POWERS, JA
    WATT, DE
    KAUFFMAN, ER
    BRICKER, A
    PHIPPS, P
    MULLERKAHLE, H
    FULTON, TR
    NG, S
    SCHUMM, JW
    BRAMAN, JC
    KNOWLTON, RG
    BARKER, DF
    CROOKS, SM
    LINCOLN, SE
    DALY, MJ
    ABRAHAMSON, J
    [J]. CELL, 1987, 51 (02) : 319 - 337