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Article

BCR-ABL kinase domain mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy?

Cell cycle (Georgetown, Tex.) - 1 Dec 2005

Lange Thoralf, Park Byung, Willis Stephanie G, Deininger Michael W N

Abstract excerpt

Patients with chronic myeloid leukemia (CML) treated with imatinib in early chronic phase tend to have durable remissions, but there is a high rate of relapse in patients with advanced disease. Mutations in the kinase domain of BCR-ABL that impair drug binding have been identified as the major mechanism of resistance. It is not known when exactly these mutations arise, but in some patients retrospective analysis...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

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Source

Identifiers

PMID: 16319529
DOI: 10.4161/cc.4.12.2261

Genes

BCR

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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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