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The hematopoietic saga of clonality in sickle cell disease

Sickle cell disease (SCD) is associated with an increased risk of vascular-occlusive events and of leukemia. Clonal hematopoiesis (CH) may increase both risks. In turn, physiologic abnormalities in SCD may modify the incidence and/or distribution of genetic alterations in CH. In a recent issue of th...

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Autores principales: Stonestrom, Aaron J., Levine, Ross L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Clinical Investigation 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884916/
https://www.ncbi.nlm.nih.gov/pubmed/35175224
http://dx.doi.org/10.1172/JCI158251
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author Stonestrom, Aaron J.
Levine, Ross L.
author_facet Stonestrom, Aaron J.
Levine, Ross L.
author_sort Stonestrom, Aaron J.
collection PubMed
description Sickle cell disease (SCD) is associated with an increased risk of vascular-occlusive events and of leukemia. Clonal hematopoiesis (CH) may increase both risks. In turn, physiologic abnormalities in SCD may modify the incidence and/or distribution of genetic alterations in CH. In a recent issue of the JCI, Liggett et al. found no difference in CH rate between individuals with versus without SCD. Here we contextualize this report and discuss the complex interplay between CH and SCD with particular attention to consequences for emerging gene therapies. We further consider the limitations in our current understanding of these topics that must be addressed in order to optimize therapeutic strategies for SCD.
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spelling pubmed-88849162022-03-08 The hematopoietic saga of clonality in sickle cell disease Stonestrom, Aaron J. Levine, Ross L. J Clin Invest Commentary Sickle cell disease (SCD) is associated with an increased risk of vascular-occlusive events and of leukemia. Clonal hematopoiesis (CH) may increase both risks. In turn, physiologic abnormalities in SCD may modify the incidence and/or distribution of genetic alterations in CH. In a recent issue of the JCI, Liggett et al. found no difference in CH rate between individuals with versus without SCD. Here we contextualize this report and discuss the complex interplay between CH and SCD with particular attention to consequences for emerging gene therapies. We further consider the limitations in our current understanding of these topics that must be addressed in order to optimize therapeutic strategies for SCD. American Society for Clinical Investigation 2022-03-01 2022-03-01 /pmc/articles/PMC8884916/ /pubmed/35175224 http://dx.doi.org/10.1172/JCI158251 Text en © 2022 Stonestrom et al. https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Commentary
Stonestrom, Aaron J.
Levine, Ross L.
The hematopoietic saga of clonality in sickle cell disease
title The hematopoietic saga of clonality in sickle cell disease
title_full The hematopoietic saga of clonality in sickle cell disease
title_fullStr The hematopoietic saga of clonality in sickle cell disease
title_full_unstemmed The hematopoietic saga of clonality in sickle cell disease
title_short The hematopoietic saga of clonality in sickle cell disease
title_sort hematopoietic saga of clonality in sickle cell disease
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884916/
https://www.ncbi.nlm.nih.gov/pubmed/35175224
http://dx.doi.org/10.1172/JCI158251
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