Person:
Duraisamy, Sekhar

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Duraisamy

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Sekhar

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Duraisamy, Sekhar
Author's Publications: search.filters.isAuthorOfPublication.821fc9a9-977b-471a-a2d7-8237dbd71ae8

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    Elafin drives poor outcome in high grade serous ovarian cancers and basal-like breast tumors
    (2014) Labidi-Galy, S. Intidhar; Clauss, Adam; Ng, Vivian; Duraisamy, Sekhar; Elias, Kevin; Piao, Hui-Ying; Bilal, Erhan; Davidowitz, Rachel A.; Lu, Yiling; Badalian-Very, Gayane; Györffy, Balázs; Kang, Un-Beom; Ficarro, Scott; Ganesan, Shridar; Mills, Gordon B.; Marto, Jarrod; Drapkin, Ronny
    High grade serous ovarian carcinoma (HGSOC) and basal-like breast cancer (BLBC) share many features including TP53 mutations, genomic instability and poor prognosis. We recently reported that Elafin is overexpressed by HGSOC and is associated with poor overall survival. Here, we confirmed that Elafin overexpression is associated with shorter survival in 1000 HGSOC patients. Elafin confers a proliferative advantage to tumor cells through activation of the MAP kinase pathway. This mitogenic effect can be neutralized by RNA interference, specific antibodies, and a MEK inhibitor. Elafin expression in patient-derived samples was also associated with chemoresistance and strongly correlates with bcl-xL expression. We extended these findings into examination of 1100 primary breast tumors and six breast cancer cell lines. We observed that Elafin is overexpressed and secreted specifically by BLBC tumors and cell lines, leading to a similar mitogenic effect through activation of the MAP kinase pathway. Here too, Elafin overexpression is associated with poor overall survival, suggesting that it may serve as a biomarker and therapeutic target in this setting.
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    The Polyoma Virus Large T Binding Protein p150 Is a Transcriptional Repressor of c-MYC
    (Public Library of Science, 2012) Sung, Chang Kyoo; Yim, Hyungshin; Gu, Hongcang; Li, Dawei; Andrews, Erik; Duraisamy, Sekhar; Li, Cheng; Drapkin, Ronny; Benjamin, Thomas
    p150, product of the SALL2 gene, is a binding partner of the polyoma virus large T antigen and a putative tumor suppressor. p150 binds to the nuclease hypersensitive element of the c-MYC promoter and represses c-MYC transcription. Overexpression of p150 in human ovarian surface epithelial cells leads to decreased expression, and downregulation to increased expression, of c-MYC. c-MYC is repressed upon restoration of p150 to ovarian carcinoma cells. Induction of apoptosis by etoposide results in recruitment of p150 to the c-MYC promoter and to repression of c-MYC. Analysis of data in The Cancer Genome Atlas shows negative correlations between SALL2 and c-MYC expression in four common solid tumor types.