ReviewOncogene2007
Transcriptional dysregulation during myeloid transformation in AML.
Review in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed.
- Long-term follow-up of cytogenetically normal CEBPA-mutated AML.Journal of hematology & oncology · 2014Trial
- Trial
- Solubility based mechanistic profiling of combinatorial drug therapy.Nature communications · 2026Article
- Integrative analysis of aging-related genes reveals CEBPA as a novel therapeutic target in non-small cell lung cancer.Cancer cell international · 2024Article
- Therapeutic targeting of leukemia stem cells in acute myeloid leukemia.Frontiers in oncology · 2023Review
- [Characteristics of N6-methyladenosine modification patterns in t(8;21) acute myeloid leukemia].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Ribosomal proteins and human diseases: molecular mechanisms and targeted therapy.Signal transduction and targeted therapy · 2021Review
- I SPI1 something needed for B cells.The Journal of experimental medicine · 2021Article
- CDK2-instigates C/EBPα degradation through SKP2 in Acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2021Article
- DNA methylation epitypes highlight underlying developmental and disease pathways in acute myeloid leukemia.Genome research · 2021Article
- Article
- Article
- Hallmarks of ribosomopathies.Nucleic acids research · 2020Review
- CEBPA-mutated leukemia is sensitive to genetic and pharmacological targeting of the MLL1 complex.Leukemia · 2019Article
- Dependence on Myb expression is attenuated in myeloid leukaemia with N-terminal CEBPA mutations.Life science alliance · 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
- Clinical Assessment and Diagnosis of Germline Predisposition to Hematopoietic Malignancies: The University of Chicago Experience.Frontiers in pediatrics · 2017Review
- Shwachman-Bodian-Diamond syndrome (SBDS) protein deficiency impairs translation re-initiation from C/EBPα and C/EBPβ mRNAs.Nucleic acids research · 2016Article
- Proteomic discovery of MNT as a novel interacting partner of E3 ubiquitin ligase E6AP and a key mediator of myeloid differentiation.Oncotarget · 2016Article
- Genomics-based Approach and Prognostic Stratification Significance of Gene Mutations in Intermediate-risk Acute Myeloid Leukemia.Chinese medical journal · 2015Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current paradigm on leukemogenesis indicates that leukemias are propagated by leukemic stem cells. The genomic events and pathways involved in the transformation of hematopoietic precursors into leukemic stem cells are increasingly understood. This concept is based on genomic mutations or functional dysregulation of transcription factors in malignant cells of patients with acute myeloid leukemia (AML). Loss of the CCAAT/enhancer binding protein-alpha (CEBPA) function in myeloid cells in vitro and in vivo leads to a differentiation block, similar to that observed in blasts from AML patients. CEBPA alterations in specific subgroups of AML comprise genomic mutations leading to dominant-negative mutant proteins, transcriptional suppression by leukemic fusion proteins, translational inhibition by activated RNA-binding proteins, and functional inhibition by phosphorylation or increased proteasomal-dependent degradation. The PU.1 gene can be mutated or its expression or function can be blocked by leukemogenic fusion proteins in AML. Point mutations in the RUNX1/AML1 gene are also observed in specific subtypes of AML, in addition to RUNX1 being the most frequent target for chromosomal translocation in AML. These data are persuasive evidence that impaired function of particular transcription factors contributes directly to the development of human AML, and restoring their function represents a promising target for novel therapeutic strategies in AML.
Indexed as
Identifiers
17934489What 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.