Defining the region(s) of deletion at 6q16-q22 in human prostate cancer

被引:45
作者
Hyytinen, ER
Saadut, R
Chen, CS
Paull, L
Koivisto, PA
Vessella, RL
Frierson, HF
Dong, JT
机构
[1] Univ Virginia, Hlth Syst, Dept Pathol, Charlottesville, VA 22908 USA
[2] Tampere Univ, Dept Clin Genet, FIN-33101 Tampere, Finland
[3] Univ Washington, Dept Urol, Seattle, WA USA
[4] Univ Virginia, Hlth Syst, Dept Biochem & Mol Genet, Charlottesville, VA USA
关键词
D O I
10.1002/gcc.10065
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Deletion of the long arm of chromosome 6 (6q) frequently occurs in many neoplasms, including carcinomas of the prostate and breast and melanoma, suggesting the location of a tumor-suppressor gene or genes at 6q. At present, however, the region of deletion has not been well defined, and the target gene of deletion remains to be identified. In this study, we analyzed 44 primary prostate cancers with 16 polymorphic markers for loss of heterozygosity (LOH) by using PCR-based techniques. We also examined 23 cell lines/xenografts of prostate cancer with 38 markers for LOH by the method of homozygosity mapping of deletion. LOH at 6q16-q22 was detected in 21 of 44 (48%) primary tumors and in 12 of 23 (52%) cell lines/xenografts. Two regions of LOH were defined. One was 7.5 cM at 6q16-q21 between markers D6S1716 and D6S1580, and the other was 4.3 cM at 6q22 between D6S261 and D6S1702. Whereas no correlation was found between LOH at 6q16-q22 and patient age at diagnosis or Gleason score, tumors at higher stage appear to have more frequent LOH. These findings suggest that deletion of 6q16-q22 is a frequent event in prostate cancer, and that the deletion originates from two distinct regions. These results should be useful in identifying the target gene(s) of deletion at 6q. (C) 2002 Wiley-Liss, Inc.
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页码:306 / 312
页数:7
相关论文
共 49 条
[1]  
*AJCC, 1997, AJCC CANC STAG MAN
[2]   Identification of genetic markers for prostatic cancer progression [J].
Alers, JC ;
Rochat, J ;
Krijtenburg, PJ ;
Hop, WCJ ;
Kranse, R ;
Rosenberg, C ;
Tanke, HJ ;
Schröder, FH ;
van Dekken, H .
LABORATORY INVESTIGATION, 2000, 80 (06) :931-942
[3]   Molecular cytogenetic analysis of prostatic adenocarcinomas from screening studies -: Early cancers may contain aggressive genetic features [J].
Alers, JC ;
Krijtenburg, PJ ;
Vis, AN ;
Hoedemaeker, RF ;
Wildhagen, MF ;
Hop, WCJ ;
van der Kwast, TH ;
Schröder, FH ;
Tanke, HJ ;
van Dekken, H .
AMERICAN JOURNAL OF PATHOLOGY, 2001, 158 (02) :399-406
[4]   Comprehensive human genetic maps: Individual and sex-specific variation in recombination [J].
Broman, KW ;
Murray, JC ;
Sheffield, VC ;
White, RL ;
Weber, JL .
AMERICAN JOURNAL OF HUMAN GENETICS, 1998, 63 (03) :861-869
[5]  
Carvalho B, 1999, GENE CHROMOSOME CANC, V26, P29
[6]   Defining a common region of deletion at 13q21 in human cancers [J].
Chen, CS ;
Brabham, WW ;
Stultz, BG ;
Frierson, HF ;
Barrett, JC ;
Sawyers, CL ;
Isaacs, JT ;
Dong, JT .
GENES CHROMOSOMES & CANCER, 2001, 31 (04) :333-344
[7]  
Cher ML, 1998, CLIN CANCER RES, V4, P1273
[8]   COMPARATIVE GENOMIC HYBRIDIZATION, ALLELIC IMBALANCE, AND FLUORESCENCE IN-SITU HYBRIDIZATION ON CHROMOSOME-8 IN PROSTATE-CANCER [J].
CHER, ML ;
MACGROGAN, D ;
BOOKSTEIN, R ;
BROWN, JA ;
JENKINS, RB ;
JENSEN, RH .
GENES CHROMOSOMES & CANCER, 1994, 11 (03) :153-162
[9]  
Cher ML, 1996, CANCER RES, V56, P3091
[10]  
Cooney KA, 1996, CANCER RES, V56, P4150