TY - JOUR
T1 - Germ line ERG haploinsufficiency defines a new syndrome with cytopenia and hematological malignancy predisposition
AU - ERG Variants Research Network
AU - Zerella, Jiarna R.
AU - Homan, Claire C.
AU - Arts, Peer
AU - Lin, Xuzhu
AU - Spinelli, Sam J.
AU - Venugopal, Parvathy
AU - Babic, Milena
AU - Brautigan, Peter J.
AU - Truong, Lynda
AU - Arriola-Martinez, Luis
AU - Moore, Sarah
AU - Hollins, Rachel
AU - Parker, Wendy T.
AU - Nguyen, Hung
AU - Kassahn, Karin S.
AU - Branford, Susan
AU - Feurstein, Simone
AU - Larcher, Lise
AU - Sicre de Fontbrune, Flore
AU - Demirdas, Serwet
AU - de Munnik, Sonja
AU - Antoine-Poirel, Hélène
AU - Brichard, Benedicte
AU - Mansour, Sahar
AU - Gordon, Kristiana
AU - Baliakas, Panagiotis
AU - Blombery, Piers
AU - Fox, Lucy C.
AU - Donadieu, Jean
AU - Rio-Machin, Ana
AU - Steinberg-Shemer, Orna
AU - Morgan, Neil V.
AU - Ngeow, Joanne Y.Y.
AU - Skokowa, Julia
AU - Pinese, Mark
AU - Cowley, Mark J.
AU - Wlodarski, Marcin W.
AU - Koppayi, Ashwin
AU - Dobbins, Sara
AU - Mutsaers, Pim G.N.J.
AU - Nichols, Kim E.
AU - Oak, Ninad
AU - DeMille, Desiree
AU - Mao, Rong
AU - Crawford, Ali
AU - McCarrier, Julie
AU - Basel, Donald
AU - Flores-Daboub, Josue
AU - Drazer, Michael W.
AU - Phillips, Kerry
N1 - Publisher Copyright:
© 2024 American Society of Hematology
PY - 2024
Y1 - 2024
N2 - The genomics era has facilitated the discovery of new genes that predispose individuals to bone marrow failure (BMF) and hematological malignancy (HM). We report the discovery of ETS-related gene (ERG), a novel, autosomal dominant BMF/HM predisposition gene. ERG is a highly constrained transcription factor that is critical for definitive hematopoiesis, stem cell function, and platelet maintenance. ERG colocalizes with other transcription factors, including RUNX family transcription factor 1 (RUNX1) and GATA binding protein 2 (GATA2), on promoters or enhancers of genes that orchestrate hematopoiesis. We identified a rare heterozygous ERG missense variant in 3 individuals with thrombocytopenia from 1 family and 14 additional ERG variants in unrelated individuals with BMF/HM, including 2 de novo cases and 3 truncating variants. Phenotypes associated with pathogenic germ line ERG variants included cytopenias (thrombocytopenia, neutropenia, and pancytopenia) and HMs (acute myeloid leukemia, myelodysplastic syndrome, and acute lymphoblastic leukemia) with onset before 40 years. Twenty ERG variants (19 missense and 1 truncating), including 3 missense population variants, were functionally characterized. Thirteen potentially pathogenic erythroblast transformation specific (ETS) domain missense variants displayed loss-of-function (LOF) characteristics, thereby disrupting transcriptional transactivation, DNA binding, and/or nuclear localization. Selected variants overexpressed in mouse fetal liver cells failed to drive myeloid differentiation and cytokine-independent growth in culture and to promote acute erythroleukemia when transplanted into mice, concordant with these being LOF variants. Four individuals displayed somatic genetic rescue by copy neutral loss of heterozygosity. Identification of predisposing germ line ERG variants has clinical implications for patient and family diagnoses, counseling, surveillance, and treatment strategies, including selection of bone marrow donors and cell or gene therapy.
AB - The genomics era has facilitated the discovery of new genes that predispose individuals to bone marrow failure (BMF) and hematological malignancy (HM). We report the discovery of ETS-related gene (ERG), a novel, autosomal dominant BMF/HM predisposition gene. ERG is a highly constrained transcription factor that is critical for definitive hematopoiesis, stem cell function, and platelet maintenance. ERG colocalizes with other transcription factors, including RUNX family transcription factor 1 (RUNX1) and GATA binding protein 2 (GATA2), on promoters or enhancers of genes that orchestrate hematopoiesis. We identified a rare heterozygous ERG missense variant in 3 individuals with thrombocytopenia from 1 family and 14 additional ERG variants in unrelated individuals with BMF/HM, including 2 de novo cases and 3 truncating variants. Phenotypes associated with pathogenic germ line ERG variants included cytopenias (thrombocytopenia, neutropenia, and pancytopenia) and HMs (acute myeloid leukemia, myelodysplastic syndrome, and acute lymphoblastic leukemia) with onset before 40 years. Twenty ERG variants (19 missense and 1 truncating), including 3 missense population variants, were functionally characterized. Thirteen potentially pathogenic erythroblast transformation specific (ETS) domain missense variants displayed loss-of-function (LOF) characteristics, thereby disrupting transcriptional transactivation, DNA binding, and/or nuclear localization. Selected variants overexpressed in mouse fetal liver cells failed to drive myeloid differentiation and cytokine-independent growth in culture and to promote acute erythroleukemia when transplanted into mice, concordant with these being LOF variants. Four individuals displayed somatic genetic rescue by copy neutral loss of heterozygosity. Identification of predisposing germ line ERG variants has clinical implications for patient and family diagnoses, counseling, surveillance, and treatment strategies, including selection of bone marrow donors and cell or gene therapy.
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U2 - 10.1182/blood.2024024607
DO - 10.1182/blood.2024024607
M3 - Article
C2 - 38991192
AN - SCOPUS:85201660038
SN - 0006-4971
JO - Blood
JF - Blood
ER -