TY - JOUR
T1 - Microsatellite instability and expression of hMLH1 and hMSH2 proteins in ovarian endometrioid cancer
AU - Liu, Jinsong
AU - Albarracin, Constance T.
AU - Chang, Ki Hong
AU - Thompson-Lanza, Jennifer A.
AU - Zheng, Wenxin
AU - Gershenson, David M.
AU - Broaddus, Russell
AU - Luthra, Rajyalakshmi
N1 - Funding Information:
This work was supported in part by Grant P01CA64602-1 from the National Cancer Institute, Institutional start-up funds, and an Institutional Research Grant and Career Development Award from MD Anderson Cancer Center SPORE on Ovarian cancer to JL. We thank Ms Valerie Dunmire and Jennifer Merino for technical assistance, Ms Carmen Salazar for imaging, and Drs Atac Baykal and Kathy Qi Cai for critical reading of the manuscript and statistical analysis. We also thank Ms Mariann Crapanzano for editorial assistance.
PY - 2004/1
Y1 - 2004/1
N2 - Microsatellite instability and loss of heterozygosity has been implicated in ovarian carcinogenesis. The reported frequency of microsatellite instability in human ovarian cancer varies significantly owing to the use of heterogeneous tumor histotypes and various microsatellite markers in different laboratories. In this study, we determined the frequency of microsatellite instability in 74 ovarian endometrioid carcinomas using four microsatellite markers (BAT25, BAT26, D5S346, D17S250), and examined hMLH1 and hMSH2 protein expression. In all, 20% of the tumors were microsatellite instability high (two or more markers showing instability) and 12% were microsatellite instability low (one marker showed instability). Loss of hMLH1 and/or hMSH2 expression was found in nine of 15 microsatellite instability-high tumors. The microsatellite instability-high phenotype tended to occur more frequently in low-grade tumors (P=0.053), but did not correlate with clinical stage. Totally, 38% of cases also displayed loss of heterozygosity at D17S250; this loss of heterozygosity was associated with high clinical stage (P=0.097). Our results indicate that both microsatellite and loss of heterozygosity at D17S250 are involved in the development of ovarian endometrioid carcinoma.
AB - Microsatellite instability and loss of heterozygosity has been implicated in ovarian carcinogenesis. The reported frequency of microsatellite instability in human ovarian cancer varies significantly owing to the use of heterogeneous tumor histotypes and various microsatellite markers in different laboratories. In this study, we determined the frequency of microsatellite instability in 74 ovarian endometrioid carcinomas using four microsatellite markers (BAT25, BAT26, D5S346, D17S250), and examined hMLH1 and hMSH2 protein expression. In all, 20% of the tumors were microsatellite instability high (two or more markers showing instability) and 12% were microsatellite instability low (one marker showed instability). Loss of hMLH1 and/or hMSH2 expression was found in nine of 15 microsatellite instability-high tumors. The microsatellite instability-high phenotype tended to occur more frequently in low-grade tumors (P=0.053), but did not correlate with clinical stage. Totally, 38% of cases also displayed loss of heterozygosity at D17S250; this loss of heterozygosity was associated with high clinical stage (P=0.097). Our results indicate that both microsatellite and loss of heterozygosity at D17S250 are involved in the development of ovarian endometrioid carcinoma.
UR - http://www.scopus.com/inward/record.url?scp=2442712044&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2442712044&partnerID=8YFLogxK
U2 - 10.1038/modpathol.3800017
DO - 10.1038/modpathol.3800017
M3 - Article
C2 - 14631366
AN - SCOPUS:2442712044
SN - 0893-3952
VL - 17
SP - 75
EP - 80
JO - Modern Pathology
JF - Modern Pathology
IS - 1
ER -