What is the primary mechanism of action of tyrosine kinase inhibitors (TKIs) in CML?

Which signaling pathway is NOT directly activated by BCR-ABL1 in CML?

What percentage of CML patients are diagnosed in the chronic phase?

Which mutation is associated with resistance to all TKIs except ponatinib?

What does an MR4 molecular response indicate in CML treatment monitoring?

Which gene is most commonly mutated in addition to BCR-ABL1 in blast-phase CML?

What defines a major molecular response (MMR) in CML?

Which adverse event is more common with second-generation TKIs compared to imatinib?

Which pathway is NOT directly targeted by BCR-ABL1 activity but is involved in CML pathogenesis through secondary mutations?

What characteristic feature distinguishes BCR-ABL1-positive CML from BCR-ABL1-negative myeloproliferative neoplasms (MPNs)?

Which additional chromosomal abnormality in Ph-positive cells is associated with a worse prognosis in CML?

In blast-phase CML, which gene mutation is often implicated in driving progression and resistance to TKIs?

Which variant BCR-ABL1 transcript is associated with a more indolent form of CML?

What is the recommended follow-up for patients who achieve a stable deep molecular response (DMR) on TKI therapy?

What is the significance of achieving an MR5 (deep molecular response) in CML?

What role does the BCR-ABL1 oncoprotein play in cytokine-independent proliferation of leukemic cells in CML?

Which mutation is most frequently observed in accelerated-phase CML and is a marker of poor prognosis?