ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013
Bim polymorphisms: influence on function and response to treatment in children with acute lymphoblastic leukemia.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Pooled it
- Genetic Determinants of Treatment-Related Bone Toxicity in Pediatric Acute Lymphoblastic Leukemia.Clinical pharmacology and therapeutics · 2026Article
- Cul5bioRxiv : the preprint server for biology · 2025Article
- Article
- Genes identified through genome-wide association studies of osteonecrosis in childhood acute lymphoblastic leukemia patients.Pharmacogenomics · 2019Article
- Influence of BCL2L11 polymorphism on osteonecrosis during treatment of childhood acute lymphoblastic leukemia.The pharmacogenomics journal · 2019Article
- Overexpression of HIF-1α contributes to melphalan resistance in multiple myeloma cells by activation of ERK1/2, Akt, and NF-κB.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Article
- [Association between BIM gene and glucocorticoid resistance in children with acute lymphoblastic leukemia].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Review
- Venetoclax responses of pediatric ALL xenografts reveal sensitivity of MLL-rearranged leukemia.Blood · 2016Article
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- Polymorphisms of the vincristine pathway and response to treatment in children with childhood acute lymphoblastic leukemia.Pharmacogenomics · 2014Article
- Identification of cis-acting elements and splicing factors involved in the regulation of BIM Pre-mRNA splicing.PloS one · 2014Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
purposeCorticosteroids induce apoptosis in the malignant lymphoid cells and are critical component of combination therapy for acute lymphoblastic leukemia (ALL). Several genome-wide microarray studies showed major implication of proapoptotic Bim in mediating corticosteroid-related resistance in leukemia cells. EXPERIMENTAL
designWe investigated Bim gene polymorphisms and their association with childhood ALL outcome, and the mechanism underlying the observed finding.
resultsLower overall survival (OS) was associated with Bim C29201T located in Bcl-2 homology 3 (BH3) domain (P = 0.01). An association remained significant in multivariate model (P = 0.007), was more apparent in high-risk patients (P = 0.004) and patients treated with dexamethasone (P = 0.009), and was subsequently confirmed in the replication patient cohort (P = 0.03). RNA analysis revealed that C29201T affects generation of γ isoforms (γ1) that lack proapoptotic BH3 domain. The phenotypic effect was minor suggesting the influence of additional factors that may act in conjunction with Bim genotype. Combined analysis with Mcl gene polymorphism (G-486T) revealed profound reduction in OS in individuals with both risk genotypes (P < 0.0005 in discovery and P = 0.002 in replication cohort) and particularly in high-risk patients (P ≤ 0.008).
conclusionsIncreased expression of prosurvival Mcl1 and presence of Bim isoforms lacking proapoptotic function might explain marked reduction of OS in a disease and dose-dependent manner in ALL patients carrying Bim- and Mcl1-risk genotypes.
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