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Abi1 loss drives prostate tumorigenesis through activation of EMT and non-canonical WNT signaling

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Date
2019-12
Authors
Nath, Disharee
Li, Xiang
Mondragon, Claudia
Post, Dawn
Chen, Ming
White, Julie R
Hryniewicz-Jankowska, Anita
Caza, Tiffany
Kuznetsov, Vladimir A
Hehnly, Heidi
Jamaspishvili, Tamara
Berman, David M
Zhang, Fan
Kung, Sonia HY
Fazli, Ladan
Gleave, Martin E
Bratslavsky, Gennady
Pandolfi, Pier Paolo
Kotula, Leszek
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(19 total)
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Journal article
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https://hdl.handle.net/10161/19322
Published Version (Please cite this version)
10.1186/s12964-019-0410-y
Publication Info
Nath, Disharee; Li, Xiang; Mondragon, Claudia; Post, Dawn; Chen, Ming; White, Julie R; ... Kotula, Leszek (2019). Abi1 loss drives prostate tumorigenesis through activation of EMT and non-canonical WNT signaling. Cell Communication and Signaling, 17(1). 10.1186/s12964-019-0410-y. Retrieved from https://hdl.handle.net/10161/19322.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Chen

Ming Chen

Associate Professor in Pathology
Our laboratory is interested in understanding the molecular and genetic events underlying cancer progression and metastasis. The focus of our work is a series of genetically engineered mouse models that faithfully recapitulate human disease. Using a combination of mouse genetics, omics technologies, cross-species analyses and in vitro approaches, we aim to identify cancer cell–intrinsic and –extrinsic mechanisms driving metastatic cancer progression, with a long
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