Journal of Nippon Medical School: Vol.69 No.3 page.235

Journal of Nippon Medical School

Select Language
in Japanese < > in English

Full Text of this Article

in English PDF (228K)

ArticleTitle Genome-Wide Screening of Laser Capture Microdissected Gastric Signet-Ring Cell Carcinomas

AuthorList Yuji Kurihara^1,2, Mohammad Ghazizadeh¹, Hideki Bo^1,2, Hajime Shimizu¹, Oichi Kawanami¹, Yukichi Moriyama², Masahiko Onda³

Affiliation ¹Department of Molecular Pathology, Institute of Gerontology, Nippon Medical School, ²Center for Digestive Diseases, Second Hospital, Nippon Medical School, ³First Department of Surgery, Nippon Medical School

Language EN

Volume 69

Issue 3

Year 2002

Page 235-242

Received December 21, 2002

Accepted December 28, 2002

Keywords comparative genomic hybridization, laser capture microdissection, gastric adenocarcinoma, signet-ring cell, DNA copy number, genetic changes, chromosome

Abstract
Gastric signet-ring cell carcinoma comprises a distinct category of gastric cancers and has been reported to have poor prognosis. In an attempt to define genetic changes involved in the pathogenesis of this lesion in an in vivo state, we isolated signet-ring cell carcinoma cells from freshly fixed smears of tumor tissues of 7 primary gastric signet-ring cell carcinomas by laser capture microdissection and applied comparative genomic hybridization (CGH) to screen for DNA sequence copy number changes. Frequent chromosomal gains were detected on 2q, 5p, 7q, 14q and 20q, each in 6/7 cases, on 9q, 12q, 17q, and 19q, each in 5/7 cases, and on 18p in 4/7 cases. Frequent losses were observed on 6p and 17p, each in 5/7 cases, on 6q, and 21p, each in 4/7 cases, and on 3p, 8p and 8q, each in 3/7 cases. Losses on 6p have rarely been observed in conventional types of gastric carcinomas reported in the literature. These data provide the first evidence for the occurrence of specific genomic aberrations in gastric signet-ring cell carcinomas. Our observation of frequent losses on 6p chromosomal arm may provide novel abnormalities of potential significance in gastric signet-ring cell carcinomas, suggesting the involvement of genes residing in this region in the genesis of the disease.

Correspondence to M. Ghazizadeh, MD, Department of Molecular Pathology, Institute of Gerontology, 1-396 Kosugi-cho, Nakahara-ku, Kawasaki 211-8533, Japan
ciem@nms.ac.jp

ArticleTitle	Genome-Wide Screening of Laser Capture Microdissected Gastric Signet-Ring Cell Carcinomas
AuthorList	Yuji Kurihara^1,2, Mohammad Ghazizadeh¹, Hideki Bo^1,2, Hajime Shimizu¹, Oichi Kawanami¹, Yukichi Moriyama², Masahiko Onda³
Affiliation	¹Department of Molecular Pathology, Institute of Gerontology, Nippon Medical School, ²Center for Digestive Diseases, Second Hospital, Nippon Medical School, ³First Department of Surgery, Nippon Medical School
Language	EN
Volume	69
Issue	3
Year	2002
Page	235-242
Received	December 21, 2002
Accepted	December 28, 2002
Keywords	comparative genomic hybridization, laser capture microdissection, gastric adenocarcinoma, signet-ring cell, DNA copy number, genetic changes, chromosome
Abstract	Gastric signet-ring cell carcinoma comprises a distinct category of gastric cancers and has been reported to have poor prognosis. In an attempt to define genetic changes involved in the pathogenesis of this lesion in an in vivo state, we isolated signet-ring cell carcinoma cells from freshly fixed smears of tumor tissues of 7 primary gastric signet-ring cell carcinomas by laser capture microdissection and applied comparative genomic hybridization (CGH) to screen for DNA sequence copy number changes. Frequent chromosomal gains were detected on 2q, 5p, 7q, 14q and 20q, each in 6/7 cases, on 9q, 12q, 17q, and 19q, each in 5/7 cases, and on 18p in 4/7 cases. Frequent losses were observed on 6p and 17p, each in 5/7 cases, on 6q, and 21p, each in 4/7 cases, and on 3p, 8p and 8q, each in 3/7 cases. Losses on 6p have rarely been observed in conventional types of gastric carcinomas reported in the literature. These data provide the first evidence for the occurrence of specific genomic aberrations in gastric signet-ring cell carcinomas. Our observation of frequent losses on 6p chromosomal arm may provide novel abnormalities of potential significance in gastric signet-ring cell carcinomas, suggesting the involvement of genes residing in this region in the genesis of the disease.
Correspondence to	M. Ghazizadeh, MD, Department of Molecular Pathology, Institute of Gerontology, 1-396 Kosugi-cho, Nakahara-ku, Kawasaki 211-8533, Japan ciem@nms.ac.jp