ArticleBlood cells, molecules & diseases2016
The role of BCL11A and HMIP-2 polymorphisms on endogenous and hydroxyurea induced levels of fetal hemoglobin in sickle cell anemia patients from southern Brazil.
Article in Blood cells, molecules & diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Genetic Variation and Sickle Cell Disease Severity: A Systematic Review and Meta-Analysis.JAMA network open · 2023Pooled it
- Global genetic modifiers of fetal hemoglobin in sickle cell disease: Systematic review and meta-analysis.iScience · 2026Article
- BCL11A and HBS1L-MYB polymorphisms, in association with hydroxyurea and sex, modulate fetal hemoglobin levels in individuals with sickle cell anemia in the western region of Bahia, Brazil.Molecular biology reports · 2026Article
- The role of hydroxyurea in modulating miRNA expression in sickle cell disease: molecular mechanisms and therapeutic implications.Annals of hematology · 2026Review
- Enhanced induction of fetal hemoglobin by the combination of decitabine with RN-1 in β-thalassemia/HbE erythroid progenitor cells.Molecular medicine (Cambridge, Mass.) · 2026Article
- Hydroxyurea reduces the levels of the fetalJournal of sickle cell disease · 2024Article
- Genetic modifiers of fetal hemoglobin affect the course of sickle cell disease in patients treated with hydroxyurea.Haematologica · 2022Article
- Single Nucleotide Polymorphisms inDiagnostics (Basel, Switzerland) · 2022Review
- Glomerular filtration rate abnormalities in sickle cell disease.Frontiers in medicine · 2022Review
- Association Between Selected Single Nucleotide Polymorphisms in Globin and Related Genes and Response to Hydroxyurea Therapy in Ghanaian Children with Sickle Cell Disease.Pharmacogenomics and personalized medicine · 2022Article
- Trienone analogs of curcuminoids induce fetal hemoglobin synthesis via demethylation atScientific reports · 2021Article
- Do Genetic Polymorphisms Affect Fetal Hemoglobin (HbF) Levels in Patients With Sickle Cell Anemia Treated With Hydroxyurea? A Systematic Review and Pathway Analysis.Frontiers in pharmacology · 2021Review
- Functional polymorphisms of BCL11A and HBS1L-MYB genes affect both fetal hemoglobin level and clinical outcomes in a cohort of children with sickle cell anemia.Annals of hematology · 2020Article
- High fetal hemoglobin level is associated with increased risk of cerebral vasculopathy in children with sickle cell disease in Mayotte.BMC pediatrics · 2020Article
- Genetic Modifiers of Fetal Haemoglobin in Sickle Cell Disease.Molecular diagnosis & therapy · 2019Review
- Hydroxyurea in the management of sickle cell disease: pharmacogenomics and enzymatic metabolism.The pharmacogenomics journal · 2018Review
- Biological impact of α genes, β haplotypes, and G6PD activity in sickle cell anemia at baseline and with hydroxyurea.Blood advances · 2018Article
- Fetal haemoglobin induction in sickle cell disease.British journal of haematology · 2018Review
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
High levels of fetal hemoglobin (HbF) reduce sickle cell anemia (SCA) morbidity and mortality. HbF levels vary considerably and there is a strong genetic component that influences HbF production. Genetic polymorphisms at three quantitative trait loci (QTL): Xmn1-HBG2, HMIP-2 and BCL11A, have been shown to influence HbF levels and disease severity in SCA. Hydroxyurea (HU) is a drug that increases HbF. We investigated the influence of single nucleotide polymorphisms (SNPs) at the Xmn1-HBG2 (rs7482144); BCL11A (rs1427407, rs4671393 and rs11886868); and HMIP-2 (rs9399137 and rs9402686) loci on baseline and HU-induced HbF levels in 111 HbSS patients. We found that both BCL11A and HMIP-2 were associated with increased endogenous levels of HbF. Interestingly, we also found that BCL11A was associated with higher induction of HbF with HU. This effect was independent of the effect of BCL11A on baseline HbF levels. Additional studies will be needed to validate these findings and explain the ample inter-individual variations in HbF levels at baseline and HU-induced in patients with SCA.
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Registered trials
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