ReviewThe Journal of experimental medicine2014
C/EBPα: critical at the origin of leukemic transformation.
Review in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 32 citations in OpenAlex.
- Fusion oncoproteins orchestrate tumorigenesis and sustain malignant progression via a positive feedback mechanism.Cell & bioscience · 2026Review
- Breathless Revelation: Unmasking Acute Myeloid Leukemia Through Acute Respiratory Failure.Cureus · 2023Article
- Targeting C/EBPα overcomes primary resistance and improves the efficacy of FLT3 inhibitors in acute myeloid leukaemia.Nature communications · 2023Article
- NF-κB: A Druggable Target in Acute Myeloid Leukemia.Cancers · 2022Review
- Aberrant DNA hydroxymethylation reshapes transcription factor binding in myeloid neoplasms.Clinical epigenetics · 2022Article
- The AML-associated K313 mutation enhances C/EBPα activity by leading to C/EBPα overexpression.Cell death & disease · 2021Article
- Preferential CEBP binding to T:G mismatches and increased C-to-T human somatic mutations.Nucleic acids research · 2021Article
- Superior efficacy of co-targeting GFI1/KDM1A and BRD4 against AML and post-MPN secondary AML cells.Blood cancer journal · 2021Article
- Trib1 promotes acute myeloid leukemia progression by modulating the transcriptional programs of Hoxa9.Blood · 2021Article
- Myeloid transformation byLife science alliance · 2021Article
- CEBPG promotes esophageal squamous cell carcinoma progression by enhancing PI3K-AKT signaling.American journal of cancer research · 2020Article
- Structural basis for effects of CpA modifications on C/EBPβ binding of DNA.Nucleic acids research · 2019Article
- [Roles of CCAAT enhancer binding protein α in acute myeloblastic leukemia].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
- NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling.Blood · 2018Article
- Review
- CCAAT/Enhancer-binding Protein α (C/EBPα) Is Important for Osteoclast Differentiation and Activity.The Journal of biological chemistry · 2016Article
- IL-17 promotes keratinocyte proliferation via the downregulation of C/EBPα.Experimental and therapeutic medicine · 2016Article
- Article
- Genetic predisposition to myelodysplastic syndrome and acute myeloid leukemia in children and young adults.Leukemia & lymphoma · 2016Article
- The deregulated expression of miR-125b in acute myeloid leukemia is dependent on the transcription factor C/EBPα.Leukemia · 2015Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a hematopoietic malignancy characterized by clonal expansion of myeloid progenitor cells. A major mechanistic theme in AML biology is the extensive collaboration among fusion oncoproteins, transcription factors, and chromatin regulators to initiate and sustain a transformed cellular state. A new study in this issue describes how the C/EBPα transcription factor is crucial for the initiation of AML induced by MLL fusion oncoproteins, but is entirely dispensable for the maintenance of established disease. These observations provide a unique glimpse into the pioneer round of regulatory events that are critical at the origin of AML formation. Furthermore, this study implies the existence of oncogene-induced positive feedback loops capable of bypassing the continuous need for certain regulators to propagate disease.
Indexed as
Identifiers
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.