Mismatch repair protein MSH2 expression and prognosis of colorectal cancer patients

被引:2
作者
Bernardo, CG
González, JJ
Sanz, L
Barbón, E
Noval, JG
Fresno, MF
Aza, J
机构
[1] Univ Oviedo, Dept Surg, Oviedo, Spain
[2] Univ Oviedo, Cent Hosp, Inst Oncol, Dept Pathol, Oviedo, Spain
关键词
mismatch repair genes; MSH2; expression; colorectal carcinoma; prognostic factors;
D O I
10.1177/172460080401900303
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Introduction and aims: The role of genetic factors in the etiology and prognosis of patients with sporadic colorectal cancer is controversial. We have therefore investigated the biological and clinicopathological influence of immunohistochemical MSH2 expression in colorectal cancer. Patients and methods: A total of 49 consecutive patients with unselected colorectal cancer operated on in our unit were included in the study. All tumors were resected and tumor specimens were evaluated for MSH2 expression. Clinicopathological data and patient survival were correlated with MSH2 staining. Uni- and multivariate analyses were performed. The minimum follow-up period was five years. Results: Curative resection was performed in 34 patients (64.9%), 14 of whom subsequently relapsed. At the end of the overall follow-up 25 (51%) patients had died, 21 of cancer-related causes. Twenty-eight patients (57.1%) were negative for MSH2 staining. Only vascular invasion was significantly correlated with MSH2 expression (lower median values; p=0.04). The overall median survival was 47.9 months (95% Cl=27-86.6%). Multivariate analysis of variables in relation to survival showed that T stage (p=0.001), N stage (p<0.001) and MSH2 expression (p=0.01) were independent factors for survival. Conclusions: Reduced MSH2 expression is frequent in unselected colorectal cancer patients. Only vascular invasion was correlated with MSH2 expression in this study. Survival was related to TN stage and MSH2 staining.
引用
收藏
页码:190 / 195
页数:6
相关论文
共 25 条
[1]  
BIONDO S, 2001, CIR ESPAN, V70, P265
[2]   APC, β-catenin and hTCF-4;: an unholy trinity in the genesis of colorectal cancer [J].
Bright-Thomas, RM ;
Hargest, R .
EUROPEAN JOURNAL OF SURGICAL ONCOLOGY, 2003, 29 (02) :107-117
[3]  
Brueckl WM, 2003, ANTICANCER RES, V23, P1773
[4]  
Chaves P, 2000, J PATHOL, V191, P355
[5]   Evidence for an age-related influence of microsatellite instability on colorectal cancer survival [J].
Farrington, SM ;
McKinley, AJ ;
Carothers, AD ;
Cunningham, C ;
Bubb, VJ ;
Sharp, L ;
Wyllie, AH ;
Dunlop, MG .
INTERNATIONAL JOURNAL OF CANCER, 2002, 98 (06) :844-850
[6]   A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS [J].
FEARON, ER ;
VOGELSTEIN, B .
CELL, 1990, 61 (05) :759-767
[7]  
GARCIAANGUIANO F, 2001, CIR ESP, V70, P267
[8]  
HERMOSO FG, 1994, CIR ESPAN, V55, P423
[9]   The genetics of colorectal cancer [J].
Howe, JR ;
Guillem, JG .
SURGICAL CLINICS OF NORTH AMERICA, 1997, 77 (01) :175-+
[10]   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