Title |
Prostate cancer ETS rearrangements switch a cell migration gene expression program from RAS/ERK to PI3K/AKT regulation
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Published in |
Molecular Cancer, March 2014
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DOI | 10.1186/1476-4598-13-61 |
Pubmed ID | |
Authors |
Nagarathinam Selvaraj, Justin A Budka, Mary W Ferris, Travis J Jerde, Peter C Hollenhorst |
Abstract |
The RAS/ERK and PI3K/AKT pathways induce oncogenic gene expression programs and are commonly activated together in cancer cells. Often, RAS/ERK signaling is activated by mutation of the RAS or RAF oncogenes, and PI3K/AKT is activated by loss of the tumor suppressor PTEN. In prostate cancer, PTEN deletions are common, but, unlike other carcinomas, RAS and RAF mutations are rare. We have previously shown that over-expression of "oncogenic" ETS transcription factors, which occurs in about one-half of prostate tumors due to chromosome rearrangement, can bypass the need for RAS/ERK signaling in the activation of a cell migration gene expression program. In this study we test the role of RAS/ERK and PI3K/AKT signaling in the function of oncogenic ETS proteins. |
X Demographics
Geographical breakdown
Country | Count | As % |
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United States | 1 | 100% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 1 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 31 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Postgraduate | 4 | 13% |
Student > Bachelor | 4 | 13% |
Researcher | 4 | 13% |
Student > Ph. D. Student | 4 | 13% |
Student > Master | 3 | 10% |
Other | 7 | 23% |
Unknown | 5 | 16% |
Readers by discipline | Count | As % |
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Biochemistry, Genetics and Molecular Biology | 13 | 42% |
Agricultural and Biological Sciences | 6 | 19% |
Medicine and Dentistry | 3 | 10% |
Computer Science | 1 | 3% |
Unknown | 8 | 26% |