Bim Polymorphisms: Influence on Function and Response to Treatment in Children with Acute Lymphoblastic Leukemia
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Abstract
Purpose: Corticosteroids 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 Design: We investigated Bim gene polymorphisms and their association with childhood ALL outcome, and the mechanism underlying the observed finding. Results: Lower overall survival (OS) was associated with BimC29201T 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). Conclusions: Increased 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. Clin Cancer Res; 19(18); 5240–9. ©2013 AACR.
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Patients with a CC allele have greater sensitivity to corticosteroid treatment and an increased incidence of osteonecrosis.
“The importance of gauging treatment dose with allelic expression is typified by patients with a CC allele having a greater sensitivity to corticosteroid treatment and an increased incidence of osteonecrosis [39].”
From Thrombospondin-1, BIM and CFH polymorphisms and response to anti-VEGF treatment in neovascular age- related macular degeneration patients (2024) · cites this paper as [39]
The Results (page unavailable) associate the BIM C29201T genotype with outcomes during corticosteroid treatment: TT patients had the lowest overall survival, including among those receiving dexamethasone. This does not establish that CC patients are more sensitive to corticosteroids—the paper reports no significant genotype-related difference in a cellular sensitivity assay—and our copy does not report osteonecrosis incidence. (LLM, conf=0.82)
Experimental — accuracy not yet measuredResponsiveness to anti-VEGF, corticosteroids, and tyrosine kinase inhibitors hinges on BIM function, with BIM polymorphisms negating effective treatment.
“Responsiveness to anti-VEGF, corticosteroids, and tyrosine kinase inhibitors hinge on BIM function, with BIM polymorphisms negating effective treatment [27, 33, 39].”
From Thrombospondin-1, BIM and CFH polymorphisms and response to anti-VEGF treatment in neovascular age- related macular degeneration patients (2024) · cites this paper as [39]
The Discussion (page unavailable) links BIM function and a BIM polymorphism to corticosteroid response in children with ALL, and reports a previously described polymorphism affecting tyrosine kinase inhibitor sensitivity. It does not address anti-VEGF treatment. Its conclusion also describes BIM variation as one component of multifactorial resistance, not as negating effective treatment. (LLM, conf=0.88)
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- Authors
- Gagné, V., Rousseau, J., Labuda, M., Sharif-Askari, B., Brukner, I., Laverdière, C., Ceppi, F., Sallan, S. E., Silverman, L. B., Neuberg, D., Kutok, J. L., Sinnett, D., & Krajinovic, M.
- Affiliations
- Brigham and Women's Hospital (US)
- Authors' Affiliations: 1Charles Bruneau Cancer Center, Research Center CHU Sainte-Justine; Departments of 2Pediatrics and 3Pharmacology, University of Montreal; 4Department of Diagnostic Medicine, Jewish General Hospital, Montreal, Quebec, Canada; Departments of 5Pediatric Oncology and 6Biostatistics and Computational Biology, Dana-Farber Cancer Institute; 7Division of Hematology/Oncology, Children's Hospital; and 8Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts
- ORCID
- Venue
- Clinical Cancer Research
- Published
- 2013-09-15
- Volume
- 19
- Issue
- 18
- Pages
- 5240-5249
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- PMC
- PMC4128417
- OpenAlex
- W2166913340
- Cited by
- 28
- References
- 56
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 1 · 2022: 1 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 3 · 2015: 1 · 2014: 7
- FWCI
- 3.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research
- National Cancer Institute (P01CA068484)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Acute Lymphoblastic Leukemia research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- acute lymphoblastic leukemia, pediatric leukemia, steroid resistance, dexamethasone, BH3 domain, apoptosis, overall survival, prognostic factors, high-risk leukemia, combination therapy
- MeSH terms
- Bcl-2-Like Protein 11, Antineoplastic Combined Chemotherapy Protocols, Child, Dexamethasone, Female, Follow-Up Studies, Humans, Male, Membrane Proteins, Neoplasm Staging, Polymorphism, Genetic, Prednisone, Prognosis, Proto-Oncogene Proteins, RNA, Messenger, Blotting, Western, Cohort Studies, Survival Rate, Apoptosis, Drug Resistance, Neoplasm, Proto-Oncogene Proteins c-bcl-2, Reverse Transcriptase Polymerase Chain Reaction, Cell Proliferation, Apoptosis Regulatory Proteins, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Real-Time Polymerase Chain Reaction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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