ArticleGenes & development2010
p53 loss promotes acute myeloid leukemia by enabling aberrant self-renewal.
Article in Genes & development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05297123 (Treatment of Acute Myeloid Leukemia With Arsenic and All-trans Retinoid Acid), which is not on this map. Cited by 107 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.
Treatment of Acute Myeloid Leukemia With Arsenic and All-trans Retinoid Acid (ATRA)
Who cites it
107 citing papers in PubMed, 169 citations in OpenAlex.
- Association of fructose-1,6-diphosphatase 1 with the progression of diabetic kidney disease.Nutrition & metabolism · 2025Article
- TP53 -Mutated Myeloid Neoplasms: 2024 Update on Diagnosis, Risk-Stratification, and Management.American journal of hematology · 2025Review
- TP53 mutations and TET2 deficiency cooperate to drive leukemogenesis and establish an immunosuppressive environment.The Journal of clinical investigation · 2025Article
- In vivo models of subclonal oncogenesis and dependency in hematopoietic malignancy.Cancer cell · 2024Article
- Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes.International journal of molecular sciences · 2024Review
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- Loss of p53 enhances the tumor-initiating potential and drug resistance of clonogenic multiple myeloma cells.Blood advances · 2023Article
- The Prognostic Value of TP53 Mutations in Adult Acute Myeloid Leukemia: A Meta-Analysis.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2023Article
- The ADAR1 editome reveals drivers of editing-specificity for ADAR1-isoforms.Nucleic acids research · 2023Article
- Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis.International journal of molecular sciences · 2023Review
- BRCA1 and TP53 codeficiency causes a PARP inhibitor-sensitive erythroproliferative neoplasm.JCI insight · 2022Article
- FBP1-Altered Carbohydrate Metabolism Reduces Leukemic Viability through Activating P53 and Modulating the Mitochondrial Quality Control System In Vitro.International journal of molecular sciences · 2022Article
- Comparison of acute myeloid leukemia and myelodysplastic syndromes with TP53 aberrations.Annals of hematology · 2022Article
- TP53 promotes lineage commitment of human embryonic stem cells through ciliogenesis and sonic hedgehog signaling.Cell reports · 2022Article
- Murine Models of Acute Myeloid Leukemia.Frontiers in oncology · 2022Review
- The Role of Tumor Stem Cell Exosomes in Cancer Invasion and Metastasis.Frontiers in oncology · 2022Review
- Review
- Review
- The Agglutinin of Common Nettle (Urtica dioica L.) Plant Effects on Gene Expression Related to Apoptosis of Human Acute Myeloid Leukemia Cell Line.Biochemical genetics · 2021Article
- RNA sequencing of long-term label-retaining colon cancer stem cells identifies novel regulators of quiescence.iScience · 2021Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor limits proliferation in response to cellular stress through several mechanisms. Here, we test whether the recently described ability of p53 to limit stem cell self-renewal suppresses tumorigenesis in acute myeloid leukemia (AML), an aggressive cancer in which p53 mutations are associated with drug resistance and adverse outcome. Our approach combined mosaic mouse models, Cre-lox technology, and in vivo RNAi to disable p53 and simultaneously activate endogenous Kras(G12D)-a common AML lesion that promotes proliferation but not self-renewal. We show that p53 inactivation strongly cooperates with oncogenic Kras(G12D) to induce aggressive AML, while both lesions on their own induce T-cell malignancies with long latency. This synergy is based on a pivotal role of p53 in limiting aberrant self-renewal of myeloid progenitor cells, such that loss of p53 counters the deleterious effects of oncogenic Kras on these cells and enables them to self-renew indefinitely. Consequently, myeloid progenitor cells expressing oncogenic Kras and lacking p53 become leukemia-initiating cells, resembling cancer stem cells capable of maintaining AML in vivo. Our results establish an efficient new strategy for interrogating oncogene cooperation, and provide strong evidence that the ability of p53 to limit aberrant self-renewal contributes to its tumor suppressor activity.
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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.