ArticleMolecular genetics & genomic medicine2022
Acute myeloid leukemia due to germline CEBPA mutation in a Syrian family.
Article in Molecular genetics & genomic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Hereditary Predisposition to Acute Myeloid Leukemia: A Novel Germline CEBPA Mutation in a Multigenerational Family.Case reports in hematology · 2026Article
- Germline CEBPA Mutation as a Rare Cause of Chronic Neutropenia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024Article
- Targeting autophagy: polydatin's role in inducing cell death in AML.Frontiers in pharmacology · 2024Article
- Sporadic and Familial Acute Myeloid Leukemia with CEBPA Mutations.Current hematologic malignancy reports · 2023Review
- Acute myeloid leukemia due to germline CEBPA mutation in a Syrian family.Molecular genetics & genomic medicine · 2022Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFamilial cases of adult acute myeloid leukemia (AML) with germline-mutated CCAAT/enhancer-binding protein-α (CEBPA) gene are a rare entity classified in World Health Organization (WHO) classification 2016. Most families reported in the literature show an autosomal dominant inheritance pattern consistent with a single-gene mutation.
methodsHere we studied a Syrian family with four individuals suffering from AML for CEBPA gene mutations by Sanger sequencing.
resultsThe father, his three affected, and one yet unaffected child had the same mutation in the N-terminal region of CEBPA (c.198dupC), resulting in termination at Tyr67Leufs*41. All affected family members had a good primary response to chemotherapy and achieved complete remission.
conclusionOverall, another AML family with CEBPA gene mutation is added to the literature, presenting with yet unreported FAB subtype M5 and absence of CD7 expression in some family members.
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