Transient erythroblastopenia due to a GATA1 variant in an infant female.

Diamond-Blackfan anemia GATA1 female lyonization transient erythroblastopenia

Journal

Pediatric blood & cancer
ISSN: 1545-5017
Titre abrégé: Pediatr Blood Cancer
Pays: United States
ID NLM: 101186624

Informations de publication

Date de publication:
27 Dec 2023
Historique:
revised: 11 12 2023
received: 09 08 2023
accepted: 16 12 2023
medline: 27 12 2023
pubmed: 27 12 2023
entrez: 27 12 2023
Statut: aheadofprint

Résumé

Diamond-Blackfan anemia (DBA) is a congenital anemia with erythroid cell aplasia. Most of the causative genes are ribosomal proteins. GATA1, a hematopoietic master transcription factor required for erythropoiesis, also causes DBA. GATA1 is located on Xp11.23; therefore, DBA develops only in males in an X-linked inheritance pattern. Here, we report a case of transient erythroblastopenia and moderate anemia in a female newborn infant with a de novo GATA1 variant. In this patient, increased methylation of the GATA1 wild-type allele was observed in erythroid cells. Skewed lyonization of GATA1 may cause mild transient erythroblastopenia in a female patient.

Identifiants

pubmed: 38149846
doi: 10.1002/pbc.30834
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e30834

Subventions

Organisme : Ministry of Health, Labor and Welfare

Informations de copyright

© 2023 Wiley Periodicals LLC.

Références

Ball S. Diamond Blackfan anemia. Hematology Am Soc Hematol Educ Program. 2011;2011:487-491.
Willig TN, Draptchinskaia N, Dianzani I, et al. Mutations in ribosomal protein S19 gene and Diamond Blackfan anemia: wide variations in phenotypic expression. Blood. 1999;94(12):4294-4306.
Gazda HT, Preti M, Sheen MR, et al. Frameshift mutation in p53 regulator RPL26 is associated with multiple physical abnormalities and a specific pre-ribosomal RNA processing defect in Diamond-Blackfan anemia. Hum Mutat. 2012;33(7):1037-1044.
Ulirsch JC, Verboon JM, Kazerounian S, et al. The genetic landscape of Diamond-Blackfan anemia. Am J Hum Genet. 2018;103(6):930-947.
Sankaran VG, Ghazvinian R, Do R, et al. Exome sequencing identifies GATA1 mutations resulting in Diamond-Blackfan anemia. J Clin Invest. 2012;122(7):2439-2443.
Klar J, Khalfallah A, Arzoo PS, Gazda HT, Dahl N. Recurrent GATA1 mutations in Diamond-Blackfan anaemia. Br J Haematol. 2014;166(6):949-951.
Ludwig LS, Gazda HT, Eng JC, et al. Altered translation of GATA1 in Diamond-Blackfan anemia. Nat Med. 2014;20(7):748-753.
Khajuria RK, Munschauer M, Ulirsch JC, et al. Ribosome levels selectively regulate translation and lineage commitment in human hematopoiesis. Cell. 2018;173(1):90-103. e119.
Au WY, Ma ES, Lam VM, Chan JL, Pang A, Kwong YL. Glucose 6-phosphate dehydrogenase (G6PD) deficiency in elderly Chinese women heterozygous for G6PD variants. Am J Med Genet A. 2004;129A(2):208-211.
Au WY, Lam V, Pang A, et al. Glucose-6-phosphate dehydrogenase deficiency in female octogenarians, nanogenarians, and centenarians. J Gerontol A Biol Sci Med Sci. 2006;61(10):1086-1089.
Camargo R, Sahoo SS, Cordoba JC, Magalhaes IQ. Germline GATA1 exon 2 mutation associated with chronic cytopenia and a non-down syndrome transient abnormal myelopoiesis with clonal trisomy 21. Leukemia. 2022;36(9):2347-2350.
Hasle H, Kline RM, Kjeldsen E, et al. Germline GATA1s-generating mutations predispose to leukemia with acquired trisomy 21 and Down syndrome-like phenotype. Blood. 2022;139(21):3159-3165.

Auteurs

Motoi Yamashita (M)

Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Takahiro Tomoda (T)

Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Ami Mizuo (A)

Department of Pediatrics, Kagawa University, Kagawa, Japan.
Department of Pediatrics, Kagawa Saiseikai Hospital, Kagawa, Japan.

Takeshi Isoda (T)

Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Makiko Egawa (M)

Department of Nutrition and Metabolism in Cardiovascular Disease, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Masayuki Yoshida (M)

Department of Nutrition and Metabolism in Cardiovascular Disease, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Tsutomu Toki (T)

Department of Pediatrics, Hirosaki University Graduate School of Medicine, Aomori, Japan.

Ko Kudo (K)

Department of Pediatrics, Hirosaki University Graduate School of Medicine, Aomori, Japan.

Kiminori Terui (K)

Department of Pediatrics, Hirosaki University Graduate School of Medicine, Aomori, Japan.

Etsuro Ito (E)

Department of Pediatrics, Hirosaki University Graduate School of Medicine, Aomori, Japan.

Tomohiro Morio (T)

Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Masatoshi Takagi (M)

Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Classifications MeSH