HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER		Author Keyword(s) Vol Page [Advanced]

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Perez-Ordonez, B Articles by Jordan, R C K Search for Related Content PubMed PubMed Citation Articles by Perez-Ordonez, B Articles by Jordan, R C K

Expression of mismatch repair proteins, ß catenin, and E cadherin in intestinal-type sinonasal adenocarcinoma

¹ Department of Pathology, University Health Network, Princess Margaret Hospital, 610 University Avenue, Room 4-304, Toronto, Ontario M4N 3M5, Canada
² Department of Pathology, Vancouver Hospital, Vancouver, British Columbia, Canada
³ University of California San Francisco, San Francisco, California, USA

Correspondence to:
Dr B Perez-Ordoñez
Department of Pathology, University Health Network, Princess Margaret Hospital, 610 University Avenue, Room 4-304, Toronto, Ontario M4N 3M5, Canada; bayardo.perez-ordonez{at}uhn.on.ca Background: Despite their histological resemblance to colorectal adenocarcinomas, there is little information about the molecular events involved in the pathogenesis of intestinal-type sinonasal adenocarcinomas (ITACs).

Aims: To evaluate the possible role of DNA mismatch repair (MMR) gene defects or disruptions of the E cadherin–ß catenin complex in ITAC by investigating the immunohistochemical expression of the MMR gene products, ß catenin, and E cadherin in a group of sporadic ITACs.

Methods: Ten sporadic cases of ITAC were stained with antibodies against MLH1, MSH2, MSH3, MSH6, ß catenin, and E cadherin.

Results: Nine cases showed strong nuclear expression of MLH1, whereas one case showed moderate staining. All 10 cases were strongly positive for MSH2 and MSH3. MSH6 was strong in nine cases, and moderate in one. Membranous ß catenin expression was strong in all 10 cases, and no case showed cytoplasmic or nuclear staining. E cadherin was strong in seven cases, and moderate in three cases.

Conclusions: The preserved nuclear expression of MLH1, MSH2, MSH3, and MSH6 suggests that mutations or promoter methylation of MMR genes do not play a role in the pathogenesis of ITAC. The strong membranous staining for E cadherin and ß catenin and lack of abnormal cytoplasmic or nuclear expression is in keeping with the preservation of E cadherin–ß catenin complexes and ß catenin pathways.

Abbreviations: APC, adenomatous polyposis coli; IHC, immunohistochemistry; ITAC, intestinal-type sinonasal adenocarcinoma; MMR, mismatch repair; MSI, microsatellite instability

Keywords: intestinal-type sinonasal adenocarcinoma; sinonasal tract; ßcatenin; Ecadherin; MLH1; MSH2