ALLELIC LOSS OF CHROMOSOME-16Q AND CHROMOSOME-10Q IN HUMAN PROSTATE-CANCER

被引:518
作者
CARTER, BS
EWING, CM
WARD, WS
TREIGER, BF
AALDERS, TW
SCHALKEN, JA
EPSTEIN, JI
ISAACS, WB
机构
[1] JOHNS HOPKINS MED INST,BRADY UROL INST RES LABS,BALTIMORE,MD 21205
[2] JOHNS HOPKINS MED INST,DEPT PATHOL,BALTIMORE,MD 21205
[3] CATHOLIC UNIV NIJMEGEN,UROL RES LABS,NIJMEGEN,NETHERLANDS
关键词
DNA polymorphism; loss of heterozygosity; tumor suppressor genes;
D O I
10.1073/pnas.87.22.8751
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Recent advances in understanding the molecular genetics of common adult tumors have indicated that multiple genetic alterations including the activation of oncogenes and the inactivation of tumor suppressor genes are important in the pathogenesis of these tumors. Loss of heterozygosity is a hallmark of tumor suppressor gene inactivation and has been used to identify chromosomal regions that contain these genes. We have examined allelic loss in the most common tumor in men, prostate cancer. Twenty-eight prostate cancer specimens have been examined for loss of heterozygosity at 11 different chromosomal arms including 3p, 7q, 9q, 10p, 10q, 11p, 13q, 16p, 16q, 17p, and 18q. Fifty-four percent (13/24) of clinically localized tumors and 4 of 4 metastatic tumors showed loss of heterozygosity on at least one chromosome. Chromosomes 16q and 10q exhibited the highest frequency of loss of heterozygosity with 30% of tumors showing loss at these chromosomes. These data demonstrate that allelic loss is a common event in prostate cancer and suggest that chromosomes 16q and 10q may contain the sites of tumor suppressor genes important in the pathogenesis of human prostate cancer.
引用
收藏
页码:8751 / 8755
页数:5
相关论文
共 49 条
[1]   CHROMOSOME STUDY OF 5 CANCERS OF THE PROSTATE [J].
ATKIN, NB ;
BAKER, MC .
HUMAN GENETICS, 1985, 70 (04) :359-364
[2]   CHROMOSOME-17 DELETIONS AND P53 GENE-MUTATIONS IN COLORECTAL CARCINOMAS [J].
BAKER, SJ ;
FEARON, ER ;
NIGRO, JM ;
HAMILTON, SR ;
PREISINGER, AC ;
JESSUP, JM ;
VANTUINEN, P ;
LEDBETTER, DH ;
BARKER, DF ;
NAKAMURA, Y ;
WHITE, R ;
VOGELSTEIN, B .
SCIENCE, 1989, 244 (4901) :217-221
[3]   SUPPRESSION OF TUMORIGENICITY OF HUMAN PROSTATE CARCINOMA-CELLS BY REPLACING A MUTATED RB GENE [J].
BOOKSTEIN, R ;
SHEW, JY ;
CHEN, PL ;
SCULLY, P ;
LEE, WH .
SCIENCE, 1990, 247 (4943) :712-715
[4]   PREVALENCE OF RAS GENE-MUTATIONS IN HUMAN COLORECTAL CANCERS [J].
BOS, JL ;
FEARON, ER ;
HAMILTON, SR ;
VERLAANDEVRIES, M ;
VANBOOM, JH ;
VANDEREB, AJ ;
VOGELSTEIN, B .
NATURE, 1987, 327 (6120) :293-297
[5]   ISOLATION AND MAPPING OF A POLYMORPHIC DNA-SEQUENCE (CTBQ7) ON CHROMOSOME-10 [D10S28] [J].
BRAGG, T ;
NAKAMURA, Y ;
JONES, C ;
WHITE, R .
NUCLEIC ACIDS RESEARCH, 1988, 16 (23) :11395-11395
[6]  
BROTHMAN AR, 1990, CANCER RES, V50, P3795
[7]   A HIGHLY POLYMORPHIC LOCUS ON CHROMOSOME-16Q REVEALED BY A PROBE FROM A CHROMOSOME-SPECIFIC COSMID LIBRARY [J].
BUFTON, L ;
MOHANDAS, TK ;
MAGENIS, RE ;
SHEEHY, R ;
BESTWICK, RK ;
LITT, M .
HUMAN GENETICS, 1986, 74 (04) :425-431
[8]   ISOLATION AND CHARACTERIZATION OF A ZINC FINGER POLYPEPTIDE GENE AT THE HUMAN CHROMOSOME-11 WILMS TUMOR LOCUS [J].
CALL, KM ;
GLASER, T ;
ITO, CY ;
BUCKLER, AJ ;
PELLETIER, J ;
HABER, DA ;
ROSE, EA ;
KRAL, A ;
YEGER, H ;
LEWIS, WH ;
JONES, C ;
HOUSMAN, DE .
CELL, 1990, 60 (03) :509-520
[9]   MUTATIONS IN HUMAN-BREAST CANCER - AN OVERVIEW [J].
CALLAHAN, R ;
CAMPBELL, G .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1989, 81 (23) :1780-1786
[10]  
CARTER BS, 1990, IN PRESS CANCER RES