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Article

Secondary fusion proteins as a mechanism of BCR::ABL1 kinase-independent resistance in chronic myeloid leukaemia.

British journal of haematology - 1 Feb 2023

Barnes Evan J, Eide Christopher A, Kaempf Andy, Bottomly Daniel, Romine Kyle A, Wilmot Beth, Saunders Dominick, McWeeney Shannon K, Tognon Cristina E, Druker Brian J

Abstract excerpt

Drug resistance in chronic myeloid leukaemia (CML) may occur via mutations in the causative BCR::ABL1 fusion or BCR::ABL1-independent mechanisms. We analysed 48 patients with BCR::ABL1-independent resistance for the presence of secondary fusion genes by RNA sequencing. We identified 10 of the most frequently detected secondary fusions in 21 patients. Validation studies, cell line models, gene expression analysis...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

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

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Share to Protein Kinase Inhibitors

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Identifiers

PMID: 36264026
DOI: 10.1111/bjh.18515
PMCID: PMC9851972

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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