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BCR-ABL, FLT3, Lyn, HCK
- Molecular classification
- Enzyme, Protein kinase, Tyrosine kinase, Receptor tyrosine kinase, Nonreceptor tyrosine kinase
01
Overview
This entry incorrectly combines multiple distinct protein kinases (BCR-ABL, FLT3, Lyn, HCK) into a single therapeutic target. While all are relevant in hematological malignancies, they are individual, unrelated protein targets that should be considered and structured separately, as their specific disease roles, interacting drugs, and biomarkers vary. This grouping violates standard target curation conventions, as each kinase represents a unique therapeutic protein.
02
Mechanism of action
ATP-competitive inhibition of tyrosine kinase activity, leading to inhibition of downstream proliferative signals and apoptosis. The specific targets and precise mechanisms vary across the individual kinases grouped in this entry.
03
Biological functions
Signal transductionCell proliferationApoptosis regulationOncogenic transformationHematopoietic cell developmentCell survivalRegulation of immune responsesSignal transduction in B cells and myeloid cellsSignal transduction in myeloid lineage cellsImmune response regulation
04
Disease associations
Cancerchronic myelogenous leukemia (CML)acute lymphoblastic leukemia (ALL)acute myeloid leukemia (AML)leukemiaslymphomasautoimmunityinflammationmyeloid leukemias
05
Safety considerations
Resistance mutations (e.g. T315I)MyelosuppressionCardiovascular events (with some TKIs)Risk of differentiation syndromeCytopeniasOff-target immune effectsPotential for immunosuppression
06
Interacting drugs
8 more in the full profile.
07
Biomarkers
BCR-ABL1 fusion transcript or protein expressionQuantitative PCR for minimal residual diseaseFLT3-ITD or FLT3-TKD mutations for patient selectionLyn activation or overexpression (in research/diagnostic contexts)HCK expression or phosphorylation status (research context)
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