| Literature DB >> 25240283 |
Ilan Weinreb1, Salvatore Piscuoglio2, Luciano G Martelotto2, Daryl Waggott3, Charlotte K Y Ng2, Bayardo Perez-Ordonez1, Nicholas J Harding4, Javier Alfaro5, Kenneth C Chu4, Agnes Viale6, Nicola Fusco7, Arnaud da Cruz Paula8, Caterina Marchio2, Rita A Sakr9, Raymond Lim2, Lester D R Thompson10, Simion I Chiosea11, Raja R Seethala11, Alena Skalova12, Edward B Stelow13, Isabel Fonseca14, Adel Assaad15, Christine How16, Jianxin Wang4, Richard de Borja4, Michelle Chan-Seng-Yue4, Christopher J Howlett17, Anthony C Nichols17, Y Hannah Wen2, Nora Katabi2, Nicholas Buchner18, Laura Mullen18, Thomas Kislinger19, Bradly G Wouters19, Fei-Fei Liu20, Larry Norton21, John D McPherson22, Brian P Rubin23, Blaise A Clarke1, Britta Weigelt2, Paul C Boutros24, Jorge S Reis-Filho25.
Abstract
Polymorphous low-grade adenocarcinoma (PLGA) is the second most frequent type of malignant tumor of the minor salivary glands. We identified PRKD1 hotspot mutations encoding p.Glu710Asp in 72.9% of PLGAs but not in other salivary gland tumors. Functional studies demonstrated that this kinase-activating alteration likely constitutes a driver of PLGA.Entities:
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Year: 2014 PMID： 25240283 DOI： 10.1038/ng.3096
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330