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• W4280493987 abstract "PharmacogenomicsVol. 23, No. 7 EditorialPharmacogenomics of hydroxyurea therapy and fetal hemoglobin levels in sickle cell anemiaRahyssa Rodrigues Sales, Bárbara Lisboa Nogueira & Marcelo Rizzatti LuizonRahyssa Rodrigues Sales *Author for correspondence: Tel.: +55 31 3409 3072; E-mail Address: rahyssar.sales@gmail.comhttps://orcid.org/0000-0001-8197-850XGraduate Program in Genetics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, 31270-901, BrazilSearch for more papers by this author, Bárbara Lisboa Nogueira https://orcid.org/0000-0002-4090-1546Graduate Program in Genetics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, 31270-901, BrazilSearch for more papers by this author & Marcelo Rizzatti Luizon https://orcid.org/0000-0002-8331-3525Graduate Program in Genetics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, 31270-901, BrazilDepartment of Genetics, Ecology & Evolution, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, 31270-901, BrazilSearch for more papers by this authorPublished Online:12 May 2022https://doi.org/10.2217/pgs-2022-0050AboutSectionsView ArticleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInRedditEmail View articleKeywords: hydroxyureapharmacogeneticspharmacogenomicssickle cell anemiaPapers of special note have been highlighted as: •• of considerable interestReferences1. Kato GJ, Piel FB, Reid CD et al. Sickle cell disease. Nat. Rev. Dis. Primers 4, 18010 (2018). •• Review article focused on sickle cell anemia that balanced the remarkable advances with the key major challenges remaining worldwide to improve its prevention and management.Crossref, Medline, Google Scholar2. Habara A, Steinberg MH. Minireview: genetic basis of heterogeneity and severity in sickle cell disease. Exp. Biol. Med. (Maywood) 241(7), 689–696 (2016).Crossref, Medline, CAS, Google Scholar3. Steinberg MH. Fetal hemoglobin in sickle cell anemia. Blood 136(21), 2392–2400 (2020). •• Review article on the importance of heterogeneity of the distribution of fetal hemoglobin (HbF) concentrations among HbF-containing erythrocytes, the expanded use of hydroxyurea and new targets for HbF induction in sickle cell disease.Crossref, Medline, Google Scholar4. Bauer DE, Orkin SH. Hemoglobin switching's surprise: the versatile transcription factor BCL11A is a master repressor of fetal hemoglobin. Curr. Opin. Genet. Dev. 33, 62–70 (2015).Crossref, Medline, CAS, Google Scholar5. Bauer DE, Kamran SC, Lessard S et al. An erythroid enhancer of BCL11A subject to genetic variation determines fetal hemoglobin level. Science 342(6155), 253–257 (2013).Crossref, Medline, CAS, Google Scholar6. Luizon MR, Ahituv N. Uncovering drug-responsive regulatory elements. Pharmacogenomics 16(16), 1829–1841 (2015). •• Review of 108 pharmacogenomic genome-wide association studies (GWASs) showing that the huge majority of the associated SNPs are located within noncoding (96.4%) regions, mostly located within intergenic (46.3%) regions, and also focusing on how regulatory elements affect drug responseLink, CAS, Google Scholar7. Farrell JJ, Sherva RM, Chen ZY et al. A 3-bp deletion in the HBS1L-MYB intergenic region on chromosome 6q23 is associated with HbF expression. Blood 117(18), 4935–4945 (2011).Crossref, Medline, CAS, Google Scholar8. Sales RR, Belisario AR, Faria G, Mendes F, Luizon MR, Viana MB. 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. Ann. Hematol. 99(7), 1453–1463 (2020). •• Comprehensive association analyses of 14 noncoding SNPs from five loci with both fetal hemoglobin levels and with several clinical outcomes in children with SCA, including the functional annotation of the noncoding SNPs.Crossref, Medline, CAS, Google Scholar9. Menzel S, Rooks H, Zelenika D et al. Global genetic architecture of an erythroid quantitative trait locus, HMIP-2. Ann. Hum. Genet. 78(6), 434–451 (2014).Crossref, Medline, CAS, Google Scholar10. Sales RR, Nogueira BL, Belisario AR et al. Fetal hemoglobin-boosting haplotypes of BCL11A gene and HBS1L-MYB intergenic region in the prediction of clinical and hematological outcomes in a cohort of children with sickle cell anemia. J. Human Genetics (2022). •• Fetal hemoglobin-boosting haplotypes formed by the combination of alleles for functional SNPs of BCL11A and HMIP-2 intergenic region are associated with less severe hematological phenotypes and lower incidence of clinical complications in children with sickle cell anemia and interact to regulate fetal hemoglobin levels.Google Scholar11. Khandros E, Huang P, Peslak SA et al. Understanding heterogeneity of fetal hemoglobin induction through comparative analysis of F and A erythroblasts. Blood 135(22), 1957–1968 (2020).Crossref, Medline, Google Scholar12. Charache S, Dover GJ, Moore RD et al. Hydroxyurea: effects on hemoglobin F production in patients with sickle cell anemia. Blood 79(10), 2555–2565 (1992).Crossref, Medline, CAS, Google Scholar13. Charache S, Terrin ML, Moore RD et al. Effect of hydroxyurea on the frequency of painful crises in sickle cell anemia. Investigators of the Multicenter Study of Hydroxyurea in Sickle Cell Anemia. N. Engl. J. Med. 332(20), 1317–1322 (1995).Crossref, Medline, CAS, Google Scholar14. McGann PT, Ware RE. Hydroxyurea therapy for sickle cell anemia. Expert Opin. Drug Saf. 14(11), 1749–1758 (2015).Crossref, Medline, CAS, Google Scholar15. Ware RE, Despotovic JM, Mortier NA et al. Pharmacokinetics, pharmacodynamics, and pharmacogenetics of hydroxyurea treatment for children with sickle cell anemia. Blood 118(18), 4985–4991 (2011).Crossref, Medline, CAS, Google Scholar16. Sales RR, Nogueira BL, Tosatti JaG, Gomes KB, Luizon MR. Do genetic polymorphisms affect fetal hemoglobin (HbF) levels in patients with sickle cell anemia treated with hydroxyurea? A systematic review and pathway analysis. Front. Pharmacol. 12, 779497 (2022). •• Systematic review including pharmacogenetic studies that found 50 different SNPs of 17 genes to be associated with fetal hemoglobin changes in patients with sickle cell anemia treated with hydroxyurea.Crossref, Medline, Google Scholar17. Kato GJ, Steinberg MH, Gladwin MT. Intravascular hemolysis and the pathophysiology of sickle cell disease. J. Clin. Invest. 127(3), 750–760 (2017). •• Review on intravascular hemolysis, a key feature of sickle cell anemia, as an intrinsic mechanism for vascular disease that manifests clinical complications in sickle cell disease.Crossref, Medline, Google Scholar18. Wonkam A, Ngo Bitoungui VJ, Vorster AA et al. Association of variants at BCL11A and HBS1L-MYB with hemoglobin F and hospitalization rates among sickle cell patients in Cameroon. PLoS One 9(3), e92506 (2014).Crossref, Medline, Google Scholar19. Wang WC, Ware RE, Miller ST et al. Hydroxycarbamide in very young children with sickle-cell anaemia: a multicentre, randomised, controlled trial (BABY HUG). Lancet 377(9778), 1663–1672 (2011).Crossref, Medline, CAS, Google Scholar20. Frati G, Miccio A. Genome editing for beta-hemoglobinopathies: advances and challenges. J. Clin. Med. 10(3), 1663–72 (2021).Crossref, Medline, Google Scholar21. Steinberg MH, Chui DH, Dover GJ, Sebastiani P, Alsultan A. Fetal hemoglobin in sickle cell anemia: a glass half full? Blood 123(4), 481–485 (2014).Crossref, Medline, CAS, Google ScholarFiguresReferencesRelatedDetails Vol. 23, No. 7 STAY CONNECTED Metrics Downloaded 77 times History Received 18 April 2022 Accepted 19 April 2022 Published online 12 May 2022 Published in print May 2022 Information© 2022 Future Medicine LtdKeywordshydroxyureapharmacogeneticspharmacogenomicssickle cell anemiaAuthor contributionsRR Sales, BL Nogueira and MR Luizon made substantial contributions to the conception or design of the work. RR Sales, BL Nogueira and MR Luizon drafted the work or revised it critically for important intellectual content. All authors read and approved the final version of the manuscript.Financial & competing interests disclosureRR Sales and BL Nogueira are supported by fellowships from the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES-Brazil). MR Luizon is supported by Research Productivity Scholarships from the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq-Brazil). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.No writing assistance was utilized in the production of this manuscript.PDF download" @default.
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