Simultaneous Inhibition of PI3Kδ and PI3Kα Induces ABC-DLBCL Regression by Blocking BCR-Dependent and -Independent Activation of NF-κB and AKT

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• 作者：Juliane Paul¹ ; ⁵ ; Maurice Soujon¹ ; ⁵ ; Antje M. Wengner¹ ; Sabine Zitzmann-Kolbe¹ ; Andrea Sturz¹ ; Katja Haike¹ ; Koh Hui Keng Magdalene² ; Sze Huey Tan³ ; Martin Lange¹ ; Soo Yong Tan² ; ⁶ ; Dominik Mumberg¹ ; Soon Thye Lim⁴ ; Karl Ziegelbauer¹ ; Ningshu Liu¹ ; ^{ningshu.liu@bayer.com}
• 关键词：PI3Kα ; PI3Kδ ; NF-κB ; BCR ; MYD88 ; CARD11 ; DLBCL ; follicular lymphoma ; ibrutinib-resistance ; copanlisib
• 刊名：Cancer Cell
• 出版年：2017
• 出版时间：9 January 2017
• 年：2017
• 卷：31
• 期：1
• 页码：64-78
• 全文大小：4635 K
• 卷排序：31

文摘

Dual PI3Kα/δ inhibition is required to block AKT and NF-κB activation in ABC-DLBCL PI3K regulates BCR-dependent and -independent NF-κB activation via p-IκBα and cIAPs PI3Kα/δ inhibitor copanlisib induced tumor regression in MYD88mut ABC-DLBCL in vivo Ibrutinib and copanlisib combination led to sustained complete response of DLBCL