ReviewCritical reviews in oncogenesis2011
C/EBPα dysregulation in AML and ALL.
Review in Critical reviews in oncogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 57 citations in OpenAlex.
- Molecular alterations in the GATA-2, RUNX1, C/EBPα and hTERT genes in patients with aplastic anemia by MLPA.Genetics and molecular biology · 2026Article
- Cebpa is required for haematopoietic stem and progenitor cell generation and maintenance in zebrafish.Open biology · 2024Article
- An Updated Overview of the Role of CYP450 during Xenobiotic Metabolization in Regulating the Acute Myeloid Leukemia Microenvironment.International journal of molecular sciences · 2023Review
- NF-κB: A Druggable Target in Acute Myeloid Leukemia.Cancers · 2022Review
- Mutations of Intrinsically Disordered Protein Regions Can Drive Cancer but Lack Therapeutic Strategies.Biomolecules · 2021Article
- An updated account on molecular heterogeneity of acute leukemia.American journal of blood research · 2021Review
- Secondary leukemia in patients with germline transcription factor mutations (RUNX1, GATA2, CEBPA).Blood · 2020Review
- TRIB2 contributes to cisplatin resistance in small cell lung cancer.Oncotarget · 2017Article
- Transcription Factor GFI1B in Health and Disease.Frontiers in oncology · 2017Review
- Article
- The presence of C/EBPα and its degradation are both required for TRIB2-mediated leukaemia.Oncogene · 2016Article
- Article
- CDC25A governs proliferation and differentiation of FLT3-ITD acute myeloid leukemia.Oncotarget · 2015Article
- C/EBPα in normal and malignant myelopoiesis.International journal of hematology · 2015Review
- Aberrant nuclear factor-kappa B activity in acute myeloid leukemia: from molecular pathogenesis to therapeutic target.Oncotarget · 2015Review
- Zinc finger protein 382 is downregulated by promoter hypermethylation in pediatric acute myeloid leukemia patients.International journal of molecular medicine · 2014Article
- The Cebpa +37-kb enhancer directs transgene expression to myeloid progenitors and to long-term hematopoietic stem cells.Journal of leukocyte biology · 2014Article
- CEBPA exerts a specific and biologically important proapoptotic role in pancreatic β cells through its downstream network targets.Molecular biology of the cell · 2014Article
- Suv39h1 mediates AP-2α-dependent inhibition of C/EBPα expression during adipogenesis.Molecular and cellular biology · 2014Article
- CEBPA-dependent HK3 and KLF5 expression in primary AML and during AML differentiation.Scientific reports · 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor CCAAT/enhancer binding protein a (C/EBPα) is a critical regulator of myeloid development, directing granulocyte, and monocyte differentiation. As such, it is dysregulated in more than half of patients with acute myeloid leukemia (AML). C/EBPα expression is suppressed as result of common leukemia-associated genetic and epigenetic alterations such as AML1-ETO, BCR-ABL, FLT3-ITD, or CEBPA promoter methylation. In addition, 10-15% of patients with AML with intermediate risk cytogenetics are characterized by mutations of the CEBPA gene. Two classes of mutations are described. N-terminal changes result in expression of a truncated dominant negative C/EBPαp30 isoform. C-terminal mutations are in-frame insertions or deletions resulting in alteration of the leucine zipper preventing dimerization and DNA binding. Often, patients carry both N- and C-terminal mutations each affecting a different allele, and a mouse model recapitulates the human phenotype. Patients with mutated CEBPA AML comprise a clinically distinct group with favorable outcome consistently seen in patients with biallelic mutations. In addition, C/EBP family members are aberrantly expressing from the immunoglobulin heavy chain locus in 2% of pre-B ALLs. This review summarizes the normal hematopoietic developmental pathways regulated by C/EBPα and discusses the molecular pathways involved in mutated CEBPA AML and ALL.
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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.