We show that NOXA deletion, but not BIM deletion, in BCL2 and BCL‐X L ‐dependent DLBCL cells both in vitro and in vivo resulted in a highly significant enhanced resistance to both BCL2i and BCL‐X L inhibitors.
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The BH3-only protein NOXA is essential for apoptosis induction by BH3-mimetics targeting BCL2 or BCL-X<sub>L</sub> in DLBCL.
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