Reduced levels of ITGB1 cause activation of p38MAPK-ERK-LYN axis of BCR::ABL1 signaling despite inactivation of the oncoprotein by imatinib – novel resistance mechanism in blast crisis of chronic myeloid leukemia unraveled
Low ITGB1 levels activate BCR::ABL1 signaling pathways leading to imatinib resistance in CML blast crisis.
Reduced ITGB1 levels activate BCR::ABL1 downstream kinases p38MAPK and ERK, leading to activation of LYN and downstream pro‑survival pathways, thereby conferring imatinib resistance in chronic myeloid leukemia blast crisis.
Demonstrates a BCR::ABL1‑independent mechanism of imatinib resistance that may guide combination therapies to improve outcomes in the blast crisis phase of chronic myeloid leukemia.
Evidence level: Sejtvonalas. Laboratóriumi sejtekben vizsgálták.
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