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Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [H. K., B. v. R., A. R. L., B. M. R., M. S. B., K. R. C., L. H.], and Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231 [F. S. L., K. R. C., L. H.]
Endometrial carcinoma is the second most common tumor type in women with hereditary nonpolyposis colorectal carcinoma. Microsatellite instability (MI) has been observed in the inherited (hereditary nonpolyposis colorectal carcinoma-associated) form of endometrial carcinoma as well as in approximately 20% of presumably sporadic cases. Recent studies suggest that MI in many cell lines or xenografts derived from sporadic colorectal carcinomas is not attributable to mutations in four known human DNA mismatch repair (MMR) genes (hMSH2, hMLH1, hPMS1, and hPMS2). Mutational analyses of these four MMR genes in endometrial carcinomas have not been previously reported. We analyzed nine sporadic MI-positive primary endometrial carcinomas for mutations in the above four MMR genes. Mutations were detected in two tumors (in hMSH2), and both of the mutations were acquired somatically. Immunohistochemical staining revealed a lack of expression of hMSH2 protein in the two tumors containing hMSH2 mutations. Our data suggest that mutations in these four known DNA MMR genes are not responsible for M1 in the majority of sporadic endometrial carcinomas displaying this phenotype.
1 This project was supported by funds from the Richard W. TeLinde Endowment and from NIH Grant R29-CA66720 (to L. H.). L. H. is the recipient of a Passano Physician Scientist Award.
2 To whom requests for reprints should be addressed, at Department of Pathology, Johns Hopkins Medical Institutions, Ross Research Building, 720 Rutland Avenue, Baltimore, MD 21205-2196; MI, microsatellite instability.
Received 9/ 1/95. Accepted 10/20/95.
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