Recurrent chromosome changes in 62 primary gastric carcinomas detected by comparative genomic hybridization

被引：53

作者：

Guan, XY

Fu, SB

Xia, JC

Fang, Y

Sham, JST

Du, BD

Zhou, H

Lu, S

Wang, BQ

Lin, YZ

Liang, QW

Li, XM

Du, B

Ning, XM

Du, JR

Li, P

Trent, JM

机构：

[1] Univ Hong Kong, Queen Mary Hosp, Dept Clin Oncol, Hong Kong, Peoples R China

[2] Harbin Med Univ, Dept Biol, Med Genet Lab, Harbin, Peoples R China

[3] Sun Yat Sen Univ Med Sci, Ctr Canc, Guangzhou, Peoples R China

[4] Normal Bethune Univ Med Sci, Teaching Hosp 1, Dept Otolaryngol Head & Neck Surg, Changchun, Peoples R China

[5] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA

[6] Harbin Med Univ, Tumor Hosp, Dept Pathol, Harbin, Peoples R China

[7] Harbin Med Univ, Affiliated Hosp 2, Dept Pathol, Harbin, Peoples R China

来源：

CANCER GENETICS AND CYTOGENETICS | 2000年 / 123卷 / 01期

关键词：

D O I：

10.1016/S0165-4608(00)00306-X

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Comparative genomic hybridization (CGH) has been applied to detect recurrent chromosome alterations in 62 primary gastric carcinomas. Several nonrandom chromosomal changes, including gains of 8q (31 cases, 50%), 20q (29 cases, 47%) with a minimum gain region at 20q11.2-q12, 13q (21 cases, 34%) with a minimum gain region at 13q22, and 3q (19 cases, 31%) were commonly observed. The regions most frequently lost included: 19p (23 cases, 37%), 37p (21 cases, 33%), and Ip (14 cases, 23%). High copy number gain (DNA sequence amplification) was detected in 6 cases. Amplification of 8q23-q24.2 and 20q11.2-q12 were observed in 3 cases. Gain of 20q and loss of 19p were confirmed by fluorescence in situ hybridization using corresponding bacterial artificial chromosomes (BAC) clones from those regions. The gain and loss of chromosomal regions identified in this study provide candidate regions involved in gastric tumorigenesis. (C) 2000 Elsevier Science Inc. All rights reserved.

引用

页码：27 / 34

页数：8

共 29 条

[1] AIB1, a steroid receptor coactivator amplified in breast and ovarian cancer [J].

Anzick, SL ;

Kononen, J ;

Walker, RL ;

Azorsa, DO ;

Tanner, MM ;

Guan, XY ;

Sauter, G ;

Kallioniemi, OP ;

Trent, JM ;

Meltzer, PS .

SCIENCE, 1997, 277 (5328) :965-968

[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] CANCER STATISTICS, 1994 [J].

BORING, CC ;

SQUIRES, TS ;

TONG, T ;

MONTGOMERY, S .

CA-A CANCER JOURNAL FOR CLINICIANS, 1994, 44 (01) :7-26

[5] Deletion mapping on chromosome 1p in well-differentiated gastric cancer [J].

Ezaki, T ;

Yanagisawa, A ;

Ohta, K ;

Aiso, S ;

Watanabe, M ;

Hibi, T ;

Kato, Y ;

Nakajima, T ;

Ariyama, T ;

Inazawa, J ;

Nakamura, Y ;

Horii, A .

BRITISH JOURNAL OF CANCER, 1996, 73 (04) :424-428

[6] K-SAM, AN AMPLIFIED GENE IN STOMACH-CANCER, IS A MEMBER OF THE HEPARIN-BINDING GROWTH-FACTOR RECEPTOR GENES [J].

HATTORI, Y ;

ODAGIRI, H ;

NAKATANI, H ;

MIYAGAWA, K ;

NAITO, K ;

SAKAMOTO, H ;

KATOH, O ;

YOSHIDA, T ;

SUGIMURA, T ;

TERADA, M .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (15) :5983-5987

[7] Localization of a susceptibility locus for Peutz-Jeghers syndrome to 19p using comparative genomic hybridization and targeted linkage analysis [J].

Hemminki, A ;

Tomlinson, I ;

Markie, D ;

Jarvinen, H ;

Sistonen, P ;

Bjorkqvist, AM ;

Knuutila, S ;

Salovaara, R ;

Bodmer, W ;

Shibata, D ;

delaChapelle, A ;

Aaltonen, LA .

NATURE GENETICS, 1997, 15 (01) :87-90

[8] Gain of chromosome 3q defines the transition from severe dysplasia to invasive carcinoma of the uterine cervix [J].

Heselmeyer, K ;

Schrock, E ;

duManoir, S ;

Blegen, H ;

Shah, K ;

Steinbeck, R ;

Auer, G ;

Ried, T .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (01) :479-484

[9] P53 MUTATIONS IN HUMAN CANCERS [J].

HOLLSTEIN, M ;

SIDRANSKY, D ;

VOGELSTEIN, B ;

HARRIS, CC .

SCIENCE, 1991, 253 (5015) :49-53

[10]

HORII A, 1992, CANCER RES, V52, P3231

← 1 2 3 →