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.

Manoel Ferreira de Magalhães Filho, Ilana Luize Rocha Santana, Pâmela Lourdes Pereira da Silva, Larissa Paola Rodrigues Venancio

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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Manoel Ferreira de Magalhães FilhoCentro das Ciências Biológicas e da Saúde (CCBS), Federal University of Western Bahia (UFOB), Barreiras, 47808-021, Bahia, Brazil.ORCID http://orcid.org/0009-0009-0545-4654

Ilana Luize Rocha SantanaInstituto de Biociências, Letras e Ciências Exatas (IBILCE), São Paulo State University (UNESP), São José do Rio Preto, São Paulo, 15054-000, Brazil.ORCID http://orcid.org/0009-0006-3504-2827

Pâmela Lourdes Pereira da SilvaCentro das Ciências Biológicas e da Saúde (CCBS), Federal University of Western Bahia (UFOB), Barreiras, 47808-021, Bahia, Brazil.ORCID http://orcid.org/0009-0006-5843-8541

Larissa Paola Rodrigues VenancioCentro das Ciências Biológicas e da Saúde (CCBS), Federal University of Western Bahia (UFOB), Barreiras, 47808-021, Bahia, Brazil. larissa.venancio@ufob.edu.br.ORCID http://orcid.org/0000-0003-1814-8954

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6 · The paper itself

Abstract

backgroundSickle cell anemia (SCA) is a condition caused by a mutation in the HBB gene, leading to the production of hemoglobin S in red blood cells. Hydroxyurea (HU), used in treatment, increases fetal hemoglobin (HbF) levels, thereby reducing erythrocyte sickling, as do single-nucleotide polymorphisms (SNPs) in the BCL11A gene and the HBS1L-MYB intergenic region. In this study, we investigated the combined effects of HU therapy, β METHODS AND

resultsThe DNA of 43 individuals with SCA was analyzed for SNPs rs4671393, rs7557939, rs1427407, and rs11886868 (BCL11A), and rs4895441, rs9402686, and rs11759553 (HBS1L-MYB). Individuals receiving HU therapy presented significantly higher HbF levels than untreated individuals (p = 0.028). Factorial ANOVA demonstrated a significant interaction between HU use, β

conclusionsThese findings reinforce the contribution of genetic variants in BCL11A and HBS1L-MYB to HbF modulation in SCA. The identification of genetic markers associated with increased HbF levels may contribute to future strategies for individualized therapeutic monitoring in SCA.

Indexed as

Anemia, Sickle CellCarrier ProteinsFetal HemoglobinGTP-Binding ProteinsHydroxyureaNuclear ProteinsPeptide Elongation FactorsPolymorphism, Single NucleotideProto-Oncogene Proteins c-mybAdolescentAdultBrazilChildFemaleHaplotypesHumansBCL11A protein, humanCarrier ProteinsFetal HemoglobinGTP-Binding ProteinsHBS1L protein, humanHydroxyureaMYB protein, humanNuclear ProteinsPeptide Elongation FactorsProto-Oncogene Proteins c-mybRepressor ProteinsBCL11AFetal hemoglobin modulationGenetic modifiersHBS1L-MYBHydroxyurea responseSickle cell anemia

Identifiers

PMID42334731

DOI10.1007/s11033-026-12151-9

PMCPMC13290901

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