{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T18:14:12Z","timestamp":1792088052603,"version":"4.4.0"},"reference-count":130,"publisher":"American Society of Hematology","issue":"21","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,11,19]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Fetal hemoglobin (HbF) can blunt the pathophysiology, temper the clinical course, and offer prospects for curative therapy of sickle cell disease. This review focuses on (1) HbF quantitative trait loci and the geography of \u03b2-globin gene haplotypes, especially those found in the Middle East; (2) how HbF might differentially impact the pathophysiology and many subphenotypes of sickle cell disease; (3) clinical implications of person-to-person variation in the distribution of HbF among HbF-containing erythrocytes; and (4) reactivation of HbF gene expression using both pharmacologic and cell-based therapeutic approaches. A confluence of detailed understanding of the molecular basis of HbF gene expression, coupled with the ability to precisely target by genomic editing most areas of the genome, is producing important preliminary therapeutic results that could provide new options for cell-based therapeutics with curative intent.<\/jats:p>","DOI":"10.1182\/blood.2020007645","type":"journal-article","created":{"date-parts":[[2020,8,17]],"date-time":"2020-08-17T19:54:38Z","timestamp":1597694078000},"page":"2392-2400","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":129,"title":["Fetal hemoglobin in sickle cell anemia"],"prefix":"10.1182","volume":"136","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8800-8020","authenticated-orcid":false,"given":"Martin H.","family":"Steinberg","sequence":"first","affiliation":[{"name":"Division of Hematology\/Oncology, Department of Medicine, Center of Excellence for Sickle Cell Disease, Center for Regenerative Medicine, Genome Science Institute, Boston University School of Medicine and Boston Medical Center, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"issue":"16","key":"2020120315415952000_B1","doi-asserted-by":"crossref","first-page":"1561","DOI":"10.1056\/NEJMra1510865","article-title":"Sickle cell disease","volume":"376","author":"Piel","year":"2017","journal-title":"N Engl J Med"},{"issue":"5","key":"2020120315415952000_B2","doi-asserted-by":"crossref","first-page":"1245","DOI":"10.1182\/blood.V70.5.1245.1245","article-title":"Hemoglobin S gelation and sickle cell disease","volume":"70","author":"Eaton","year":"1987","journal-title":"Blood"},{"issue":"26","key":"2020120315415952000_B3","doi-asserted-by":"crossref","first-page":"15018","DOI":"10.1073\/pnas.1922004117","article-title":"Allosteric control of hemoglobin S fiber formation by oxygen and its relation to the pathophysiology of sickle cell 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