ArticleLeukemia2012
Overexpression of wild-type or mutants forms of CEBPA alter normal human hematopoiesis.
Article in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- What Is Acute Myeloid Leukemia?EJHaem · 2025Review
- A system-level model reveals that transcriptional stochasticity is required for hematopoietic stem cell differentiation.NPJ systems biology and applications · 2024Article
- Role of microRNAs and their downstream target transcription factors in zebrafish thrombopoiesis.Scientific reports · 2023Article
- Role of MicroRNAs and their Downstream Target Transcription Factors in Zebrafish Thrombopoiesis.Research square · 2023Article
- Review
- The molecular landscape of pediatric acute myeloid leukemia reveals recurrent structural alterations and age-specific mutational interactions.Nature medicine · 2018Article
- Highly efficient genome editing of human hematopoietic stem cells via a nano-silicon-blade delivery approach.Integrative biology : quantitative biosciences from nano to macro · 2017Article
- The presence of C/EBPα and its degradation are both required for TRIB2-mediated leukaemia.Oncogene · 2016Article
- CEBPA methylation and mutation in myelodysplastic syndrome.Medical oncology (Northwood, London, England) · 2015Article
- Positional cloning and next-generation sequencing identified a TGM6 mutation in a large Chinese pedigree with acute myeloid leukaemia.European journal of human genetics : EJHG · 2015Article
- Transcriptional fine-tuning of microRNA-223 levels directs lineage choice of human hematopoietic progenitors.Cell death and differentiation · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
CCAAT/enhancer-binding protein-α (C/EBPα/CEBPA) is mutated in approximately 8% of acute myeloid leukemia (AML) in both familial and sporadic AML and, with FLT3 and NPM1, has received most attention as a predictive marker of outcome in patients with normal karyotype disease. Mutations clustering to either the N- or C-terminal (N- and C-ter) portions of the protein have different consequences on the protein function. In familial cases, the N-ter form is inherited with patients exhibiting long latency period before the onset of overt disease, typically with the acquisition of a C-ter mutation. Despite the essential insights murine models provide the functional consequences of wild-type C/EBPα in human hematopoiesis and how different mutations are involved in AML development have received less attention. Our data underline the critical role of C/EBPα in human hematopoiesis and demonstrate that C/EBPα mutations (alone or in combination) are insufficient to convert normal human hematopoietic stem/progenitor cells into leukemic-initiating cells, although individually each altered normal hematopoiesis. It provides the first insight into the effects of N- and C-ter mutations acting alone and to the combined effects of N/C double mutants. Our results mimicked closely what happens in CEBPA mutated patients.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.