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

نویسندگان

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

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.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Amplification of the BRCA2 pathway gene EMSY in sporadic breast cancer is related to negative outcome.

DNA amplification at band q13 of chromosome 11 is common in breast cancer, and CCND1 and EMS1 remain the strongest candidate genes. However, amplification patterns are consistent with the existence of four cores of amplification, suggesting the involvement of additional genes. Here we present evidence strongly suggesting the involvement of the recently characterized EMSY gene in the formation o...

متن کامل

The Breast Cancer Oncogene EMSY Represses Transcription of Antimetastatic microRNA miR-31

Amplification of the EMSY gene in sporadic breast and ovarian cancers is a poor prognostic indicator. Although EMSY has been linked to transcriptional silencing, its mechanism of action is unknown. Here, we report that EMSY acts as an oncogene, causing the transformation of cells in vitro and potentiating tumor formation and metastatic features in vivo. We identify an inverse correlation betwee...

متن کامل

EMSY Links the BRCA2 Pathway to Sporadic Breast and Ovarian Cancer

The BRCA2 gene is mutated in familial breast and ovarian cancer, and its product is implicated in DNA repair and transcriptional regulation. Here we identify a protein, EMSY, which binds BRCA2 within a region (exon 3) deleted in cancer. EMSY is capable of silencing the activation potential of BRCA2 exon 3, associates with chromatin regulators HP1beta and BS69, and localizes to sites of repair f...

متن کامل

Genetic and epigenetic alterations of familial pancreatic cancers.

BACKGROUND Little is known about the genetic and epigenetic changes that contribute to familial pancreatic cancers. The aim of this study was to compare the prevalence of common genetic and epigenetic alterations in sporadic and familial pancreatic ductal adenocarcinomas. METHODS DNA was isolated from the microdissected cancers of 39 patients with familial and 36 patients with sporadic pancre...

متن کامل

The EMSY threonine 207 phospho-site is required for EMSY-driven suppression of DNA damage repair

BRCA1 and BRCA2 are essential for the repair of double-strand DNA breaks, and alterations in these genes are a hallmark of breast and ovarian carcinomas. Other functionally related genes may also play important roles in carcinogenesis. Amplification of EMSY, a putative BRCAness gene, has been suggested to impair DNA damage repair by suppressing BRCA2 function. We employed direct repeat GFP (DR-...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • International journal of clinical and experimental pathology

دوره 1 4  شماره 

صفحات  -

تاریخ انتشار 2008