Inhibition of glutaminase-1 in DLBCL potentiates venetoclax-induced antitumor activity by promoting oxidative stress.

"Conflict-of-interest disclosure: G.L. has participated in a consulting or advisory role not related to the results of this study for AbbVie, ADC Therapeutics, Amgen, AstraZeneca, Bayer, Bristol Myers Squibb, Constellation, Gilead, Genase, Genmab, Hexal/Sandoz, Immagene, Incyte, Janssen, Karyopharm, Lilly, Miltenyi, MorphoSys, NanoString, Novartis, PentixaPharm, Roche, Sobi, and Takeda; has been on a speaker’s bureau for Bayer, Celgene, Gilead, Janssen and Roche; and has received research funding not related to this study from Aquinox, AstraZeneca, Bayer, Celgene, Gilead, Janssen, and Roche. The remaining authors declare no competing financial interests."

"This work was supported by the Collaborative Research Center Transregio SFB/TR 156 (S.H.) and the 10.13039/501100005972Deutsche Krebshilfe (G.L. and S.H.)."