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DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis

Growing molecular evidence shows that uterine carcinosarcomas are clonal tumors. The carcinoma component has a dominant effect in the aggressive clinical behavior of these tumors. Defective DNA mismatch repair affects up to 30% of endometrial adenocarcinomas. The frequency and importance of defectiv...

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Bibliographic Details
Published in:Modern pathology 2006-10, Vol.19 (10), p.1333-1338
Main Authors: Taylor, Nicholas P, Zighelboim, Israel, Huettner, Phyllis C, Powell, Matthew A, Gibb, Randall K, Rader, Janet S, Mutch, David G, Edmonston, Tina B, Goodfellow, Paul J
Format: Article
Language:English
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Summary:Growing molecular evidence shows that uterine carcinosarcomas are clonal tumors. The carcinoma component has a dominant effect in the aggressive clinical behavior of these tumors. Defective DNA mismatch repair affects up to 30% of endometrial adenocarcinomas. The frequency and importance of defective DNA mismatch repair in the histiogenesis of uterine carcinosarcomas remains controversial. We studied the pattern and frequency of defective DNA mismatch repair and TP53 alterations in the epithelial and mesenchymal components of 28 uterine carcinosarcomas. We found evidence of defective DNA mismatch repair in six cases (21%) with a concordance rate of 83% for carcinoma-sarcoma pairs (κ=0.887, P
ISSN:0893-3952
1530-0285
DOI:10.1038/modpathol.3800654