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Hotspot activating PRKD1 somatic mutations in polymorphous low-grade adenocarcinomas of the salivary glands
- Weinreb, Ilan;
- Piscuoglio, Salvatore;
- Martelotto, Luciano G;
- Waggott, Daryl;
- Ng, Charlotte KY;
- Perez-Ordonez, Bayardo;
- Harding, Nicholas J;
- Alfaro, Javier;
- Chu, Kenneth C;
- Viale, Agnes;
- Fusco, Nicola;
- da Cruz Paula, Arnaud;
- Marchio, Caterina;
- Sakr, Rita A;
- Lim, Raymond;
- Thompson, Lester DR;
- Chiosea, Simion I;
- Seethala, Raja R;
- Skalova, Alena;
- Stelow, Edward B;
- Fonseca, Isabel;
- Assaad, Adel;
- How, Christine;
- Wang, Jianxin;
- de Borja, Richard;
- Chan-Seng-Yue, Michelle;
- Howlett, Christopher J;
- Nichols, Anthony C;
- Wen, Y Hannah;
- Katabi, Nora;
- Buchner, Nicholas;
- Mullen, Laura;
- Kislinger, Thomas;
- Wouters, Bradly G;
- Liu, Fei-Fei;
- Norton, Larry;
- McPherson, John D;
- Rubin, Brian P;
- Clarke, Blaise A;
- Weigelt, Britta;
- Boutros, Paul C;
- Reis-Filho, Jorge S
- et al.
Published Web Location
https://doi.org/10.1038/ng.3096Abstract
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.
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