Article
TMEM30A loss-of-function mutations drive lymphomagenesis and confer therapeutically exploitable vulnerability in B-cell lymphoma.
Nature medicine - 1 Apr 2020
Ennishi Daisuke, Healy Shannon, Bashashati Ali, Saberi Saeed, Hother Christoffer, Mottok Anja, Chan Fong Chun, Chong Lauren, Abraham Libin, Kridel Robert, Boyle Merrill, Meissner Barbara, Aoki Tomohiro, Takata Katsuyoshi, Woolcock Bruce W, Viganò Elena, Gold Michael, Molday Laurie L, Molday Robert S, Telenius Adele, Li Michael Y, Wretham Nicole, Dos Santos Nancy, Wong Mark, Viller Natasja N, Uger Robert A, Duns Gerben, Baticados Abigail, Madero Angel, Bristow Brianna N, Farinha Pedro, Slack Graham W, Ben-Neriah Susana, Lai Daniel, Zhang Allen W, Salehi Sohrab, Shulha Hennady P, Chiu Derek S, Mostafavi Sara, Gerrie Alina S, Huang Da Wei, Rushton Christopher, Villa Diego, Sehn Laurie H, Savage Kerry J, Mungall Andrew J, Weng Andrew P, Bally Marcel B, Morin Ryan D, Cohen Freue Gabriela V, Staudt Louis M, Connors Joseph M, Marra Marco A, Shah Sohrab P, Gascoyne Randy D, Scott David W, Steidl Christian
Abstract excerpt
Transmembrane protein 30A (TMEM30A) maintains the asymmetric distribution of phosphatidylserine, an integral component of the cell membrane and 'eat-me' signal recognized by macrophages. Integrative genomic and transcriptomic analysis of diffuse large B-cell lymphoma (DLBCL) from the British Columbia population-based registry uncovered recurrent biallelic TMEM30A loss-of-function mutations, which were associated...
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