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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 correspondence 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 correspondence 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
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