bioRxivGeneticsPreprint
Clonal hematopoiesis in individuals with ANKRD26 or ETV6 germline mutations
Michael William DrazeriD, Claire C. HomaniD, Kai YuiD, Marcela Cavalcante de Andrade SilvaiD, Kelsey E. McNeelyiD, Matthew J. Pozsgai, Maria Acevedo, Jeremy P. SegaliD, Peng WangiD, Jinghua FengiD, Sarah L. King‐Smith, Erika Kim, Sophia C. KoroteviD, David LawrenceiD, ANDREAS W. SCHREIBERiD, Christopher Norman HahniD, Hamish S. ScottiD, Raman B. SoodiD, NISC Comparative Sequencing Program, Elvira Deolinda Rodrigues Pereira VellosoiD, Anna L BrowniD, Paul LiuiD, Lucy A. GodleyiD
Abstract
Currently, there are at least a dozen recognized hereditary hematopoietic malignancies (HHMs), some of which phenocopy others. Among these, three HHMs driven by germline mutations in ANKRD26, ETV6, or RUNX1 share a phenotype of thrombocytopenia, qualitative platelet defects, and an increased lifetime risk of hematopoietic malignancies (HMs). Prior work has demonstrated that RUNX1 germline mutation carriers experience an elevated lifetime risk (66%) for developing clonal hematopoiesis (CH) prior to age 50. Germline mutations in ANKRD26 or ETV6 phenocopy RUNX1 germline mutations, but no studies have focused on the risk of CH in individuals with germline mutations in ANKRD26 or ETV6. To determine the prevalence of CH in individuals with germline mutations in ANKRD26 or ETV6, we performed next generation sequencing on hematopoietic tissue from twelve individuals with either germline ANKRD26 or germline ETV6 mutations. Each patient had thrombocytopenia but had not developed HMs. Among the seven individuals with germline ANKRD26 mutations, one patient had a CH clone driven by a somatic SF3B1 mutation (p.Lys700Glu). This mutation increased from a variant allele frequency (VAF) of 9.4% at age 56 to 17.4% at age 60. None of the germline ETV6 mutation carriers had evidence of CH at the limits of detection of the NGS assay (5% VAF). Unlike individuals with germline mutations in RUNX1, no individuals under the age of 50 with germline mutations in ANKRD26 or ETV6 had detectable CH. This work demonstrates that ANKRD26 germline mutation carriers, but not ETV6 mutation carriers, experience elevated risk for CH.
- organism: human
- assay: whole-exome sequencing
- research focus: differential expression
- approach: statistical model
- Citations
- 0
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Genome-wide characterization of clonal hematopoiesis reveals extensive non-coding putative driver mutations
Joshua S. Weinstock, Karen N. Conneely, … Cameron Russell·medRxiv·Oct 12, 2025
- Multi-ancestry analysis of 791K whole genomes reveals the genetic, geographic, and phenotypic correlates of somatic passenger mutations in blood
Prarthana S. Reddy, Karen N. Conneely, Joshua S. Weinstock·medRxiv·Aug 25, 2026
- Shared and distinct genetic etiologies for different types of clonal hematopoiesis
Derek W. Brown, Liam D. Cato, … Mitchell J. Machiela·Nature CommunicationsPeer-reviewed·Sep 8, 2023
- Genomic Landscape of Patients with Germline RUNX1 Variants and Familial Platelet Disorder with Myeloid Malignancies in a Natural History Study
Kai Yu, Natalie T Deuitch, … Paul Liu·Blood AdvancesPeer-reviewed·Nov 29, 2023
- Peripheral blood somatic mosaicism and clonal hematopoiesis across ancestry backgrounds
Christelle Colin, Yi-Han Tang, … Nancy Gillis·medRxiv·Mar 21, 2025
- Monogenic and polygenic inheritance become instruments for clonal selection
Po‐Ru Loh, Giulio Genovese, Steven A. McCarroll·NaturePeer-reviewed·Jun 24, 2020