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Int J Clin Exp Pathol. 2008 Jan 01;1(4):343-51.

Amplification of EMSY gene in a subset of sporadic pancreatic adenocarcinomas.

International journal of clinical and experimental pathology

W Arnout van Hattem, Ralph Carvalho, Ang Li, G Johan A Offerhaus, Michael Goggins

Affiliations

  1. Departments of Oncology Center, The Sol Goldman Pancreatic Research Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Pathology, Academic Medical Center, Amsterdam, the Netherlands, and the University Medical Center, Utrecht, the Netherlands.

PMID: 18787609 PMCID: PMC2480540

Abstract

Mutations in the breast cancer susceptibility gene 2 (BRCA2) are commonly found in familial pancreatic cancer. Recently, EMSY (11q13.5) has been described as a BRCA2 interacting protein capable of binding and inactivating the protein domain encoded by exon 3 of the BRCA2 gene. Amplification of EMSY occurs in 13% of sporadic breast cancers and is directly linked to increased expression. Here we investigate the amplification status of this new potential oncogene in 59 sporadic pancreatic cancers using fluorescence in situ hybridization (FISH) and tissue microarray (TMA). Real-time quantitative RT-PCR was performed on 20 pancreatic cancer cell lines and overexpression was calculated using the delta-delta-Ct-method. Amplification of EMSY was found in 8/59 cases (13.6%). 9/20 (45%) cell line samples showed overexpression of EMSY. In conclusion, sporadic pancreatic cancer shows amplification of EMSY at prevalence similar to that found in other cancers.

Keywords: BRCA2; EMSY; FISH; Pancreatic cancer; amplification

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