A recent breakthrough therapy combining the BCL‐2 inhibitor venetoclax with hypomethylating agents (HMAs) targeting DNA methyltransferase has improved outcomes for patients with acute myeloid leukemia (AML), but the responses and… Click to show full abstract
A recent breakthrough therapy combining the BCL‐2 inhibitor venetoclax with hypomethylating agents (HMAs) targeting DNA methyltransferase has improved outcomes for patients with acute myeloid leukemia (AML), but the responses and long‐term survival in older/unfit patients and in patients with relapsed/refractory AML remain suboptimal. Recent studies showed that inhibition of BCL‐2 or DNA methyltransferase modulates AML T‐cell immunity.
               
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