Target intelligence / Profile preview

Breakpoint Cluster Region-Abelson Tyrosine Kinase

Molecular classification
Non-receptor tyrosine kinase, Fusion protein, Enzyme
01

Overview

BCR-ABL kinase is a constitutively active, chimeric tyrosine kinase formed by the fusion of the breakpoint cluster region (BCR) gene and the Abelson murine leukemia viral oncogene homolog 1 (ABL1) gene. This fusion, resulting from the Philadelphia chromosome translocation, leads to uncontrolled cell proliferation and reduced apoptosis in leukemic cells. It is a key therapeutic target in chronic myeloid leukemia (CML) and some cases of acute lymphoblastic leukemia (ALL). Mutations within the BCR-ABL kinase domain are a major mechanism underlying resistance to tyrosine kinase inhibitors (TKIs).

Other names
BCR-ABLBCR/ABL fusion proteinPhiladelphia chromosome tyrosine kinase
02

Mechanism of action

Tyrosine kinase inhibitors (TKIs) bind to the ATP-binding site of BCR-ABL, preventing its autophosphorylation and downstream signaling.

03

Biological functions

Cell proliferationSignal transductionTyrosine phosphorylationRegulation of apoptosisRegulation of cell cycle
04

Disease associations

CancerChronic Myeloid Leukemia (CML)Acute Lymphoblastic Leukemia (ALL)Chronic Neutrophilic Leukemia (CNL)
05

Safety considerations

Development of resistance due to kinase domain mutationsCardiovascular side effects (e.g., QT prolongation)MyelosuppressionPleural effusionGastrointestinal disturbances
06

Interacting drugs

5 more in the full profile.

07

Biomarkers

BCR-ABL transcript levels (qPCR)BCR-ABL fusion gene presence (FISH)BCR-ABL kinase domain mutations

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