Does MSI-low exist?

被引:92
作者
Tomlinson, I
Halford, S
Aaltonen, L
Hawkins, N
Ward, R
机构
[1] Imperial Canc Res Fund, Mol & Populat Genet Lab, London WC2A 3PX, England
[2] John Radcliffe Hosp, Inst Mol Med, Imperial Canc Res Fund, Canc Immunogenet Lab, Oxford OX3 9DZ, England
[3] Univ Helsinki, Biomedicum Helsinki, Dept Med Genet, Finnish Canc Inst, FIN-00014 Helsinki, Finland
[4] Univ New S Wales, Sch Pathol, Sydney, NSW 2052, Australia
[5] St Vincents Hosp, Dept Med Oncol, Darlinghurst, NSW 2010, Australia
关键词
microsatellite instability; MSI-low; MSI-L; microsatellite stable; MSS; colorectal cancer;
D O I
10.1002/path.1071
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Microsatellite instability is a well-recognised phenomenon. Ten to 15% of sporadic colorectal cancers with a high level of NISI form a well defined group with distinct clinicopathological features. The set of tumours with low level of microsatellite instability (MSI-low), though widely referred to, is not a clearly defined group. The definitions of MSI-low have varied among groups and between different studies from the same group. Some studies have found associations between the NISI-L phenotype and molecular features, notably a higher frequency of K-ras mutations, and, possibly, methylation of methylguanine methyltransferase. Two recent independent studies, however, showed respectively that 68% and 79%, non-MSI-H cancers showed some MSI and could therefore be classed nominally as MSI-L. There was no evidence for a qualitatively discrete NISI-L group, but quantitative differences in the level of NISI were found. Copyright (C) 2002 John Wiley Sons, Ltd.
引用
收藏
页码:6 / 13
页数:8
相关论文
共 47 条
[11]  
Gebert J, 2000, INT J ONCOL, V16, P169
[12]   Standardized approach for microsatellite instability detection in colorectal carcinomas [J].
González-García, I ;
Moreno, V ;
Navarro, M ;
Martí-Ragué, J ;
Marcuello, E ;
Benasco, C ;
Campos, O ;
Capellà, G ;
Peinado, MA .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2000, 92 (07) :544-549
[13]   Tumor microsatellite instability and clinical outcome in young patients with colorectal cancer [J].
Gryfe, R ;
Kim, H ;
Hsieh, ETK ;
Aronson, MD ;
Holowaty, EJ ;
Bull, SB ;
Redston, M ;
Gallinger, S .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (02) :69-77
[14]  
Halford S, 2002, CANCER RES, V62, P53
[15]   Microsatellite instability and 8p allelic imbalance in stage B2 and C colorectal cancers [J].
Halling, KC ;
French, AJ ;
McDonnell, SK ;
Burgart, LJ ;
Schaid, DJ ;
Peterson, BJ ;
Moon-Tasson, L ;
Mahoney, MR ;
Sargent, DJ ;
O'Connell, MJ ;
Witzig, TE ;
Farr, GH ;
Goldberg, RM ;
Thibodeau, SN .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1999, 91 (15) :1295-1303
[16]   Colorectal carcinomas arising in the hyperplastic polyposis syndrome progress through the chromosomal instability pathway [J].
Hawkins, NJ ;
Gorman, P ;
Tomlinson, IPM ;
Bullpitt, P ;
Ward, RL .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 157 (02) :385-392
[17]   DNA microsatellite instability in hyperplastic polyps, serrated adenomas, and mixed polyps: a mild mutator pathway for colorectal cancer? [J].
Iino, H ;
Jass, JR ;
Simms, LA ;
Young, J ;
Leggett, B ;
Ajioka, Y ;
Watanabe, H .
JOURNAL OF CLINICAL PATHOLOGY, 1999, 52 (01) :5-9
[18]   UBIQUITOUS SOMATIC MUTATIONS IN SIMPLE REPEATED SEQUENCES REVEAL A NEW MECHANISM FOR COLONIC CARCINOGENESIS [J].
IONOV, Y ;
PEINADO, MA ;
MALKHOSYAN, S ;
SHIBATA, D ;
PERUCHO, M .
NATURE, 1993, 363 (6429) :558-561
[19]  
Jass JR, 2001, J PATHOL, V193, P283, DOI 10.1002/1096-9896(200103)193:3<283::AID-PATH799>3.0.CO
[20]  
2-9