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| IJCEP Copyright © 2007-All rights reserved. |
| International Journal of Clinical and Experimental Pathology |
Int J Clin Exp Pathol 1(4):343-351;2008
Original Article
Amplification of EMSY Gene in a Subset of Sporadic Pancreatic Adenocarcinomas
W. Arnout van Hattem, Ralph Carvalho, Ang Li, G. Johan A. Offerhaus and Michael Goggins
Departments of Pathology, Medicine and Oncology Center, The Sol Goldman Pancreatic Research Center, The Johns Hopkins University
School of Medicine, Baltimore, Maryland; USA; the Department of Pathology, Academic Medical Center, Amsterdam, the Netherlands, and
the University Medical Center, Utrecht, the Netherlands
Received 10 Aug 2007; accepted with revision 28 Aug 2007; available online 1 January 2008
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. (IJCEP708006).
Key Words: Pancreatic cancer, EMSY, BRCA2, FISH, amplification
Full Text PDF
Address all correspondences to: Michael Goggins, MD, Departments of Pathology, Medicine, and Oncology, The Sol Goldman
Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, 1550 Orleans St., Baltimore, MD, Tel (410)-955-3511; Fax
(410)-614-0671, Email: mgoggins@jhmi.edu
Original Article
Amplification of EMSY Gene in a Subset of Sporadic Pancreatic Adenocarcinomas
W. Arnout van Hattem, Ralph Carvalho, Ang Li, G. Johan A. Offerhaus and Michael Goggins
Departments of Pathology, Medicine and Oncology Center, The Sol Goldman Pancreatic Research Center, The Johns Hopkins University
School of Medicine, Baltimore, Maryland; USA; the Department of Pathology, Academic Medical Center, Amsterdam, the Netherlands, and
the University Medical Center, Utrecht, the Netherlands
Received 10 Aug 2007; accepted with revision 28 Aug 2007; available online 1 January 2008
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. (IJCEP708006).
Key Words: Pancreatic cancer, EMSY, BRCA2, FISH, amplification
Full Text PDF
Address all correspondences to: Michael Goggins, MD, Departments of Pathology, Medicine, and Oncology, The Sol Goldman
Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, 1550 Orleans St., Baltimore, MD, Tel (410)-955-3511; Fax
(410)-614-0671, Email: mgoggins@jhmi.edu