ArticleLeukemia research2016
Resistance to imatinib in patients with chronic myelogenous leukemia and the splice variant BCR-ABL1(35INS).
Article in Leukemia research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- From fatal disease to functional cure: 25 years of tyrosine kinase inhibition in chronic myeloid leukemia.Leukemia · 2026Review
- GOLDEN fusion: a graph-oriented learning with domain-embedding network fusion for generating super gene sets in functional genomics.Briefings in bioinformatics · 2026Article
- IGF2BP3/m6A-mediated intron retention isoform of DUSP6 promotes cisplatin resistance in nasopharyngeal carcinoma by inhibiting pyroptosis.BMC cancer · 2026Article
- Review
- The roles of non-coding RNAs (ncRNAs) in the function of leukemic stem cells (LSCs): a comprehensive review.Discover oncology · 2025Review
- A CML Patient Carrying BCR::ABL1 Splicing Variants Did Not Experience Blast Crisis for 15 Years without Responding to Various TKIs.Internal medicine (Tokyo, Japan) · 2025Article
- Targeting splicing for hematological malignancies therapy.BMC genomics · 2024Review
- Endothelium as a Source of Cardiovascular Toxicity From Antitumor Kinase Inhibitors.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- BCR::ABL1 Proteolysis-targeting chimeras (PROTACs): The new frontier in the treatment of PhLeukemia · 2024Review
- Biological relevance of alternative splicing in hematologic malignancies.Molecular medicine (Cambridge, Mass.) · 2024Review
- Long non-coding RNAs regulate treatment outcome in leukemia: What have we learnt recently?Cancer medicine · 2023Review
- BCR-ABL triggers a glucose-dependent survival program during leukemogenesis through the suppression of TXNIP.Cell death & disease · 2023Article
- Alternative RNA splicing defects in pediatric cancers: new insights in tumorigenesis and potential therapeutic vulnerabilities.Annals of oncology : official journal of the European Society for Medical Oncology · 2022Review
- KIAA1429 regulates alternative splicing events of cancer-related genes in hepatocellular carcinoma.Frontiers in oncology · 2022Article
- Multi-omics approach to identifying isoform variants as therapeutic targets in cancer patients.Frontiers in oncology · 2022Review
- Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia-From Molecular Mechanisms to Clinical Relevance.Cancers · 2021Review
- Spectrum of BCR-ABL Mutations and Treatment Outcomes in Ethiopian Imatinib-Resistant Patients With Chronic Myeloid Leukemia.JCO global oncology · 2021Article
- Roles and mechanisms of alternative splicing in cancer - implications for care.Nature reviews. Clinical oncology · 2020Review
- Tyrosine kinase inhibitors induce alternative spliced BCR-ABLCancer science · 2020Article
- Effects of dasatinib on CD8The Journal of international medical research · 2020Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
purposeIn patients with chronic myelogenous leukemia (CML), point mutations in the BCR-ABL1 kinase domain are the most common cause of treatment failure with a tyrosine kinase inhibitor (TKI). It is not clear whether the splice variant BCR-ABL1(35INS) is also associated with treatment failure. PATIENTS AND
methodsWe reviewed all CML patients who had BCR-ABL1 kinase mutation analysis performed between August 1, 2007, and January 15, 2014. Patients who had BCR-ABL1(35INS) detected had their medical records reviewed to determine response to TKI therapy.
resultsTwo hundred and eighty four patients had kinase mutation testing performed; of these, 64 patients (23%) had BCR-ABL1(35INS) detected. Forty-five patients were in chronic phase (70%), 10 were in accelerated phase (16%), 6 were in blastic phase (9%), and 3 were in other settings (5%). Of the 34 chronic phase patients who began therapy with imatinib, 23 patients (68%) failed therapy: 8 patients (24%) had primary refractory disease, 11 patients (32%) progressed, and 4 patients (12%) had disease progression after dose interruption. In contrast to the patients with disease progression or lack of response, none of 23 patients who were responding to imatinib had BCR-ABL1(35INS) detected. DNA sequencing of commonly mutated spliceosomal genes SF3B1, U2AF1, SRSF2, ZRSR2, SFA31, PRPF408, U2A565, and SF1 did not reveal mutations in seven BCR-ABL1(35INS) -positive patients tested.
conclusionsThe splice variant BCR-ABL1(35INS) is frequently found in patients who are resistant to imatinib. Mutations in the commonly mutated spliceosomal proteins do not contribute to this association.
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