Functional substitution of imatinib-inactivated canonical oncoprotein BCR::ABL1 by overexpressed PLAG1 results in BCR::ABL1-independent resistance in blast phase of chronic myeloid leukemia.
Inactivation of oncogenic BCR::ABL1 by imatinib in the early chronic phase (CP) of chronic myeloid leukemia (CML) has achieved unprecedented clinical success, which eludes the majority of terminal blast crisis (BC) patients, predominantly due to the scantily understood BCR::ABL1-independent mechanism/s of resistance. O...