ArticlePloS one2013
A single nucleotide polymorphism in cBIM is associated with a slower achievement of major molecular response in chronic myeloid leukaemia treated with imatinib.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pooled it
- Trial
- Genetic Determinants of Treatment-Related Bone Toxicity in Pediatric Acute Lymphoblastic Leukemia.Clinical pharmacology and therapeutics · 2026Article
- Review
- Understanding drug resistance in chronic myeloid leukemia through the lens of leukemic stem cell states: insights from single-cell analyses.Haematologica · 2026Review
- Bim Expression Influences Choroidal Endothelial Cell Characteristics and Their Response to Therapeutic Intervention.International journal of molecular sciences · 2024Article
- Alterations in pharmacogenetic genes and their implications for imatinib resistance in Chronic Myeloid Leukemia patients from an admixed population.Cancer chemotherapy and pharmacology · 2024Article
- Article
- Bim Expression Promotes the Clearance of Mononuclear Phagocytes during Choroidal Neovascularization, Mitigating Scar Formation in Mice.Life (Basel, Switzerland) · 2022Article
- Proapoptotic protein BIM as a novel prognostic marker in mantle cell lymphoma.Human pathology · 2019Article
- Exome, transcriptome and miRNA analysis don't reveal any molecular markers of TKI efficacy in primary CML patients.BMC medical genomics · 2019Article
- Influence of BCL2L11 polymorphism on osteonecrosis during treatment of childhood acute lymphoblastic leukemia.The pharmacogenomics journal · 2019Article
- Article
- Regulatory network analysis of microRNAs and genes in imatinib-resistant chronic myeloid leukemia.Functional & integrative genomics · 2017Article
- Differential Impacts of Alternative Splicing Networks on Apoptosis.International journal of molecular sciences · 2016Review
- The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics.Cancer discovery · 2015Review
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeBIM is essential for the response to tyrosine-kinase inhibitors (TKI) in chronic myeloid leukaemia (CML) patients. Recently, a deletion polymorphism in intron 2 of the BIM gene was demonstrated to confer an intrinsic TKI resistance in Asian patients. The present study aimed at identifying mutations in the BIM sequence that could lead to imatinib resistance independently of BCR-ABL mutations. EXPERIMENTAL
designBIM coding sequence analysis was performed in 72 imatinib-treated CML patients from a French population of our centre and in 29 healthy controls (reference population) as a case-control study. Real-time quantitative PCR (RT qPCR) was performed to assess Bim expression in our reference population.
resultsNo mutation with amino-acid change was found in the BIM coding sequence. However, we observed a silent single nucleotide polymorphism (SNP) c465C>T (rs724710). A strong statistical link was found between the presence of the T allele and the high Sokal risk group (p = 0.0065). T allele frequency was higher in non responsive patients than in the reference population (p = 0.0049). Similarly, this T allele was associated with the mutation frequency on the tyrosine kinase domain of BCR-ABL (p<0.001) and the presence of the T allele significantly lengthened the time to achieve a major molecular response (MMR). Finally, the presence of the T allele was related to a decreased basal expression of the Bim mRNA in the circulating mononuclear cells of healthy controls.
conclusionThese results suggest that the analysis of the c465C>T SNP of BIM could be useful for predicting the outcome of imatinib-treated CML patients.
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