| Literature DB >> 27015438 |
Cheng Liu1, Renee L Gallagher, Gareth R Price, Elizabeth Bolton, Christopher Joy, James Harraway, Deon J Venter, Jane E Armes.
Abstract
Microcystic stromal tumor (MST) is a rare tumor of presumed sex-cord stromal differentiation. We present a case of MST arising within a patient with constitutional 5q deletion syndrome, whose deletion encompassed the APC gene. Genomic analysis of the MST revealed a point mutation in the remaining APC allele, predicted to result in abnormal splicing of Exon 7. Subsequent clinical investigation revealed multiple gastrointestinal polyps qualifying for a diagnosis of familial adenomatous polyposis. This case emphasizes the importance of an aberrant Wnt/β-catenin pathway in the development of MST and adds credence to the inclusion of MST as a rare phenotype of familial adenomatous polyposis. In a search for additional genetic aberrations which may contribute to the development of this rare tumor, genomic analysis revealed a frameshift mutation in FANCD2, a protein which plays a key role in DNA repair. This protein is expressed in human ovarian stromal cells and FANCD2-knockout mice are known to develop sex cord-stromal tumors, factors which further support a possible role of aberrant FANCD2 in the development of MST.Entities:
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Year: 2016 PMID: 27015438 DOI: 10.1097/PGP.0000000000000289
Source DB: PubMed Journal: Int J Gynecol Pathol ISSN: 0277-1691 Impact factor: 2.762