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Article

Mechanisms of resistance to BCR-ABL TKIs and the therapeutic strategies: A review.

Critical reviews in oncology/hematology - 1 Mar 2015

Yang Ke, Fu Li-wu

Abstract excerpt

BCR-ABL caused by the translocation of t(9,22) with elevated tyrosine-kinase activity could induce leukemia in mice, which established BCR-ABL as the molecular pathogenic event in CML (Chronic myeloid leukemia). In recent years, a variety of tyrosine kinase inhibitors (TKIs) targeting at BCR-ABL specifically and effectively have been developed, which has fundamentally promoted the treatment of CML. However, the...

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Share to Antineoplastic Agents
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Fusion Proteins, bcr-abl

Share to Gene Expression Regulation, Leukemic

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

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Source

Identifiers

PMID: 25500000
DOI: 10.1016/j.critrevonc.2014.11.001

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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