ZBTB33 Is Mutated in Clonal Hematopoiesis and Myelodysplastic Syndromes and Impacts RNA Splicing

NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium; , for the Exome Aggregation Consortium,

Résultats de recherche: Contribution à un journalArticleRevue par des pairs

19 Citations (Scopus)

Résumé

Clonal hematopoiesis results from somatic mutations in cancer driver genes in hematopoietic stem cells. We sought to identify novel drivers of clonal expansion using an unbiased analysis of sequencing data from 84,683 persons and identified common mutations in the 5-methylcytosine reader ZBTB33 as well as in YLPM1, SRCAP, and ZNF318. We also identified these mutations at low frequency in patients with myelodysplastic syndrome. Zbtb33-edited mouse hematopoietic stem and progenitor cells exhibited a competitive advantage in vivo and increased genome-wide intron retention. ZBTB33 mutations potentially link DNA methylation and RNA splicing, the two most commonly mutated pathways in clonal hematopoiesis and myelodysplastic syndromes.

langue originaleAnglais
Pages (de - à)500-517
Nombre de pages18
journalBlood Cancer Discovery
Volume2
Numéro de publication5
Les DOIs
étatPublié - 1 sept. 2021
Modification externeOui

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