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Article

BCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia patients on imatinib.

Blood - 28 Oct 2010

Sherbenou Daniel W, Hantschel Oliver, Kaupe Ines, Willis Stephanie, Bumm Thomas, Turaga Lalita P, Lange Thoralf, Dao Kim-Hien, Press Richard D, Druker Brian J, Superti-Furga Giulio, Deininger Michael W

Abstract excerpt

Point mutations in the kinase domain of BCR-ABL are the most common mechanism of drug resistance in chronic myeloid leukemia (CML) patients treated with ABL kinase inhibitors, including imatinib. It has also been shown in vitro that mutations outside the kinase domain in the neighboring linker, S...

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Share to Benzamides
Share to Fusion Proteins, bcr-abl
Share to Imatinib Mesylate

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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

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Source

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Identifiers

PMID: 20519627
DOI: 10.1182/blood-2008-10-183665
PMCID: PMC2995357

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20519627-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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