Expression of hMSH2 and hMLH1 proteins of the human DNA mismatch repair system in salivary gland tumors.
BACKGROUND
The human DNA mismatch repair (hMMR) system plays an important role in reducing mutation and maintaining genomic stability. The MMR system in human cells is composed of at least six genes (hMSH2, hMLH1, hMSH3, hPMS1, hPMS2 and GTBP/hMSH6). In particular, hMSH2 and hMLH1 are expressed in cells undergoing rapid renewal; their reduced expression has been reported in several tumors.


METHODS
We examined the expression of hMSH2 and hMLH1 by immunohistochemistry in tumor specimens from 43 patients with primary tumors.


RESULTS
All carcinomas (n = 20) expressed these proteins. In addition, when compared to pleomorphic adenomas, malignant tumors contained significantly (P < 0.01) higher proportions of hMSH2 (56.1 +/- 31.5 vs. 31.1 +/- 22.6) and hMLH1 (27.9 +/- 26.0 vs. 14.0 +/- 12.6) positive cells. Warthin's tumors showed no specific nuclear staining of tumor cells for both hMSH2 and hMLH1.


CONCLUSIONS
These data suggest a minor, if any, role for a defect in the hMMR system in the pathogenesis of malignant salivary gland tumors.
Castrilli
Graziella
G
Department of Oncology, University of Chieti, Chieti, Italy.
Fabiano
Alfredo
A
La Torre
Giampiero
G
Marigo
Luca
L
Piantelli
Chiara
C
Perfetti
Giorgio
G
Ranelletti
Franco O
FO
Piantelli
Mauro
M
D048868:Adaptor Proteins, Signal Transducing; D000230:Adenocarcinoma / Q000235:genetics / Q000473:pathology; D000235:Adenolymphoma / Q000235:genetics / Q000473:pathology; D008949:Adenoma, Pleomorphic / Q000235:genetics / Q000473:pathology; D000251:Adenosine Triphosphatases / Q000032:analysis* / Q000235:genetics; D020137:Base Pair Mismatch / Q000235:genetics*; D018267:Carcinoma, Acinar Cell / Q000235:genetics / Q000473:pathology; D003528:Carcinoma, Adenoid Cystic / Q000235:genetics / Q000473:pathology; D018277:Carcinoma, Mucoepidermoid / Q000235:genetics / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000473:pathology; D002352:Carrier Proteins; D002467:Cell Nucleus / Q000648:ultrastructure; D004260:DNA Repair / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000032:analysis* / Q000235:genetics; D005347:Fibroblasts / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein; D009363:Neoplasm Proteins / Q000032:analysis* / Q000235:genetics; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins / Q000032:analysis / Q000235:genetics*; D018987:Salivary Ducts / Q000473:pathology; D012468:Salivary Gland Neoplasms / Q000235:genetics / Q000473:pathology*; D018709:Statistics, Nonparametric
D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; D004268:DNA-Binding Proteins; D019394:Ki-67 Antigen; C501486:MLH1 protein, human; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D000251:Adenosine Triphosphatases; C497172:MSH2 protein, human; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein