Inhibition of BCL2A1 by STAT5 inactivation overcomes resistance to targeted therapies of FLT3-ITD/D835 mutant AML

• Published in: Translational oncology Vol. 18; p. 101354
• Main Authors: Yamatani, Kotoko, Ai, Tomohiko, Saito, Kaori, Suzuki, Koya, Hori, Atsushi, Kinjo, Sonoko, Ikeo, Kazuho, Ruvolo, Vivian, Zhang, Weiguo, Mak, Po Yee, Kaczkowski, Bogumil, Harada, Hironori, Katayama, Kazuhiro, Sugimoto, Yoshikazu, Myslinski, Jered, Hato, Takashi, Miida, Takashi, Konopleva, Marina, Hayashizaki, Yoshihide, Carter, Bing Z., Tabe, Yoko, Andreeff, Michael
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.04.2022; Neoplasia Press; Elsevier
• Subjects: AML; BCL2A1; CAGE; FLT3; Original Research; Venetoclax; AML; CAGE; BCL2A1; FLT3; Venetoclax

•BCL2A1 is upregulated and exerts a pro-survival function in FLT3-ITD/D835 AML cells.•Upregulation of BCL2A1 attenuates sensitivity to quizartinib in FLT3-ITD/D835 cells.•Gilteritinib decreases BCL2A1 through inactivation of STAT5 in FLT3-ITD/D835 cells.•Gilteritinib/Venetoclax has a synergistic ant...