ArticleProceedings of the National Academy of Sciences of the United States of America2006
Absence of the transcription factor CCAAT enhancer binding protein alpha results in loss of myeloid identity in bcr/abl-induced malignancy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 66 citations in OpenAlex.
- ID1 in hematopoiesis and hematologic disorders: novel potentials of a classic differentiation regulator.Cellular & molecular biology letters · 2025Review
- Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution.Nature genetics · 2023Article
- Article
- The telomere complex and the origin of the cancer stem cell.Biomarker research · 2021Review
- The AML-associated K313 mutation enhances C/EBPα activity by leading to C/EBPα overexpression.Cell death & disease · 2021Article
- Molecular Landscapes and Models of Acute Erythroleukemia.HemaSphere · 2021Review
- De-regulated STAT5A/miR-202-5p/USP15/Caspase-6 regulatory axis suppresses CML cell apoptosis and contributes to Imatinib resistance.Journal of experimental & clinical cancer research : CR · 2020Article
- [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
- Loss of p53 induces leukemic transformation in a murine model of Jak2 V617F-driven polycythemia vera.Oncogene · 2017Article
- Genome-Wide Identification of Basic Helix-Loop-Helix and NF-1 Motifs Underlying GR Binding Sites in Male Rat Hippocampus.Endocrinology · 2017Article
- The presence of C/EBPα and its degradation are both required for TRIB2-mediated leukaemia.Oncogene · 2016Article
- The Philadelphia chromosome in leukemogenesis.Chinese journal of cancer · 2016Review
- Review
- Inhibitor of differentiation 1 transcription factor promotes metabolic reprogramming in hepatocellular carcinoma cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Article
- C/EBPα in normal and malignant myelopoiesis.International journal of hematology · 2015Review
- The gene signature in CCAAT-enhancer-binding protein α dysfunctional acute myeloid leukemia predicts responsiveness to histone deacetylase inhibitors.Haematologica · 2014Article
- Initiation of MLL-rearranged AML is dependent on C/EBPα.The Journal of experimental medicine · 2014Article
- C/EBPα: critical at the origin of leukemic transformation.The Journal of experimental medicine · 2014Review
- Discovery and preliminary SAR of bisbenzylisoquinoline alkaloids as inducers of C/EBPα.Bioorganic & medicinal chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The lineage-determining transcription factor CCAAT enhancer binding protein alpha (C/EBPalpha) is required for myeloid differentiation. Decreased function or expression of C/EBPalpha is often found in human acute myeloid leukemia. However, the precise impact of C/EBPalpha deficiency on the maturation arrest in leukemogenesis is not well understood. To address this question, we used a murine transplantation model of a bcr/abl-induced myeloproliferative disease. The expression of bcr/abl in C/EBPalphapos fetal liver cells led to a chronic myeloid leukemia-like disease. Surprisingly, bcr/abl-expressing C/EBPalpha-/- fetal liver cells failed to induce a myeloid disease in transplanted mice, but caused a fatal, transplantable erythroleukemia instead. Accordingly, increased expression of the transcription factors SCL and GATA-1 in hematopoietic precursor cells of C/EBPalpha-/-R01-EY-11298 ) fetal livers was found. The mechanism for the lineage shift from myeloid to erythroid leukemia was studied in a bcr/abl-positive cell line. Consistent with findings of the transplant model, expression of C/EBPalpha and GATA-1 was inversely correlated. Id1, an inhibitor of erythroid differentiation, was identified as a critical direct target of C/EBPalpha. Down-regulation of Id1 by RNA interference impaired C/EBPalpha-induced granulocytic differentiation. Taken together, our study provides evidence that myeloid lineage identity of malignant hematopoietic progenitor cells requires the residual expression of C/EBPalpha.
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.