Frequent gain of copy number on the long arm of chromosome 3 in human cervical adenocarcinoma

被引:63
作者
Yang, YC
Shyong, WY
Chang, MS
Chen, YJ
Lin, CH
Huang, ZD
Wang, TY
Hsu, MT
Chen, ML
机构
[1] Mackay Mem Hosp, Dept Med Res, Taipei 251, Taiwan
[2] Mackay Mem Hosp, Dept Obstet & Gynecol, Taipei 251, Taiwan
[3] Natl Yang Ming Univ, Dept Microbiol & Immunol, Sect 2, Taipei 112, Taiwan
[4] Mackay Mem Hosp, Dept Pathol, Taipei 251, Taiwan
[5] Natl Yang Ming Univ, Inst Biochem, Taipei 112, Taiwan
关键词
D O I
10.1016/S0165-4608(01)00510-6
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We analyzed genomic aberrations in 20 cervical adenocarcinomas by comparative genomic hybridization (CGH). Most tissue samples (85%) showed DNA copy number changes; gains were more common than losses. The most consistent region of chromosomal gain was mapped to chromosome arm 3q, found in 70% of the cases, with a minimal common region of 3q28 similar to ter. Other recurrent amplifications of genetic material were detected on 17q (45%), 1p (30%), 1q (25%), and 11q (20%). High-level copy number increases were found in chromosomal regions 3q27 similar to ter and 9pter similar to 13. DNA losses were seldom observed, occurring primarily in underrepresented regions of chromosome arms 4q, 13q, and 18q. The presence of high-risk human papilloma virus genomes in the cervical adenocarcinoma samples was detected in 90% of the cases. However, there was no correlation between human papilloma virus type and the pattern of genomic changes. This study is the first report of CGH analysis in human cervical adenocarcinoma. Among the major genomic alterations, our results demonstrate the importance of DNA copy increases of chromosome arm 3q in the development of cervical adenocarcinoma and identify other amplified chromosomal regions that are also associated with cervical carcinogenesis. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:48 / 53
页数:6
相关论文
共 40 条
  • [1] [Anonymous], IARC MON EV CARC RIS
  • [2] Arnold N, 1996, GENE CHROMOSOME CANC, V16, P46, DOI 10.1002/(SICI)1098-2264(199605)16:1<46::AID-GCC7>3.0.CO
  • [3] 2-3
  • [4] Barbati A, 1997, ANTICANCER RES, V17, P401
  • [5] Bockmuhl U, 1996, CANCER RES, V56, P5325
  • [6] INCREASED T-CELL APOPTOSIS AND TERMINAL B-CELL DIFFERENTIATION-INDUCED BY INACTIVATION OF THE ETS-1 PROTOONCOGENE
    BORIES, JC
    WILLERFORD, DM
    GREVIN, D
    DAVIDSON, L
    CAMUS, A
    MARTIN, P
    STEHELIN, D
    ALT, FW
    [J]. NATURE, 1995, 377 (6550) : 635 - 638
  • [7] QUANTITATIVE-ANALYSIS OF COMPARATIVE GENOMIC HYBRIDIZATION
    DUMANOIR, S
    SCHROCK, E
    BENTZ, M
    SPEICHER, MR
    JOOS, S
    RIED, T
    LICHTER, P
    CREMER, T
    [J]. CYTOMETRY, 1995, 19 (01): : 27 - 41
  • [8] Fu Y, 1989, PATHOLOGY UTERINE CE, P288
  • [9] Gansauge S, 1997, CANCER RES, V57, P1634
  • [10] Han SW, 1997, J SURG ONCOL, V65, P22, DOI 10.1002/(SICI)1096-9098(199705)65:1<22::AID-JSO5>3.0.CO