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BioMed Research International
Volume 2013 (2013), Article ID 396272, 10 pages
http://dx.doi.org/10.1155/2013/396272
Research Article

Molecular and Survival Differences between Familial and Sporadic Gastric Cancers

1Division of General Surgery, Department of Surgery, Taipei Veterans General Hospital, 201 Section 2, Shih-Pai Road, Taipei 11217, Taiwan
2Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan
3Division of Colorectal Surgery, Department of Surgery, Taipei Veterans General Hospital, 201 Section 2, Shih-Pai Road, Taipei 11217, Taiwan
4National Yang-Ming University, Taipei, Taiwan
5National Yang-Ming University Hospital, 152 Xin-Min Road, Yilan 26042, Taiwan
6Department of Pathology, Taipei Veterans General Hospital, 201 Section 2, Shih-Pai Road, Taipei 11217, Taiwan
7Department of Medical Research and Education, Taipei Veterans General Hospital, 201 Section 2, Shih-Pai Road, Taipei 11217, Taiwan
8Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan

Received 11 October 2012; Revised 27 December 2012; Accepted 24 January 2013

Academic Editor: Ozgur Cogulu

Copyright © 2013 Wen-Liang Fang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Mismatch repair (MMR) and germline E-cadherin (CDH1) mutations are two of the major pathways of carcinogenesis in familial gastric cancer (GC). A total of 260 sporadic and 66 familial GC patients were enrolled and molecular and survival differences were compared. Familial GC patients had earlier onset and were diagnosed at an earlier stage and had both a better 5-year overall survival rate and 3-year disease-free survival rate compared with sporadic GC patients. Only in diffuse type GC, the MSI-H phenotype and abnormal MMR protein expression were significantly higher in familial GC than in sporadic GC. In MSI-H GC, MLH1 promoter methylation was slightly higher in sporadic GC than familial GC (50% versus 23.1%), while the frequency of MMR gene mutation was slightly higher in familial GC than in sporadic GC (15.4% versus 3.1%). All of the patients with MMR gene mutation had diffuse type GC. Among familial GC patients with CDH1 mutation, most patients (72.3%) had diffuse type GC. In summary, for familial GC patients, we recommend screening of MSI status and CDH1 mutation especially for diffuse type GC. Because of the low incidence, mutation analysis of MMR gene might be considered in MSI-H familial GC with diffuse type only.