ReviewGenes, chromosomes & cancer2019
The role of TP53 in acute myeloid leukemia: Challenges and opportunities.
Review in Genes, chromosomes & cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The potential diagnosis role of TP53 mutation in advanced bladder cancer: A meta-analysis.Journal of clinical laboratory analysis · 2021Pooled it
- Solubility based mechanistic profiling of combinatorial drug therapy.Nature communications · 2026Article
- Functional heterogeneity of TP53 mutants in venetoclax-resistant AML: mechanisms, clinical implications, and therapeutic opportunities.Frontiers in oncology · 2026Review
- Article
- Therapeutic innovations: targeting ROS production in AML with natural and synthetic compounds.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Article
- Evidence-based risk stratification of myeloid neoplasms harboring TP53 mutations.Blood advances · 2025Article
- The IRF2-INPP4B Pathway Aggravates Acute Myeloid LeukemiaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2025Article
- Validation of the 5th edition of the World Health Organization and International Consensus Classification guidelines for TP53-mutated myeloid neoplasm in an independent international cohort.Blood cancer journal · 2025Article
- Iron overload mediates cytarabine resistance in AML by inhibiting the TP53 signaling pathway.Acta biochimica et biophysica Sinica · 2025Article
- Review
- Application of a high-throughput swarm-based deep neural network Algorithm reveals SPAG5 downregulation as a potential therapeutic target in adult AML.Functional & integrative genomics · 2025Article
- Establishment of two pathomic-based machine learning models to predict CLCA1 expression in colon adenocarcinoma.PloS one · 2025Article
- Hotspot gene mutations and treatment response in myelodysplastic syndromes (MDS): predictive biomarkers and targeted strategies.Frontiers in medicine · 2025Review
- Article
- Patients withCancers · 2024Article
- DCAF15 control of cohesin dynamics sustains acute myeloid leukemia.Nature communications · 2024Article
- Evaluation of the genetic basis of familial-associated early-onset hematologic cancers in an ancestral/ethnically diverse population.Haematologica · 2024Article
- Ubiquitin-specific protease 7 inhibitors reveal a differentiated mechanism of p53-driven anti-cancer activity.iScience · 2024Article
- Myelodysplasia-related gene mutations are associated with favorable prognosis in patients with TP53-mutant acute myeloid leukemia.Annals of hematology · 2024Article
9 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
4 authors.
Funding
Abstract
The tumor suppressor gene TP53 is one of the most frequently mutated genes in human cancer. The central role of the TP53 protein in several fundamental processes such as cancer, aging, senescence, and DNA repair has ensured enormous attention. However, the role of TP53 in acute myeloid leukemia (AML) is enigmatic. Unlike many other human cancers, a vast majority of AMLs display no genomic TP53 alterations. There is now growing appreciation of the fact that the unaltered TP53 status of tumor cells can be exploited therapeutically. As most AMLs have an intact TP53 gene, its physiological tumor-suppressive roles could be harnessed. Therefore, the use of pharmacological activators of the TP53 pathway may provide clinical benefit in AML. Conversely, even though the frequency of TP53 mutations in AML is substantially lower than in other human cancers, TP53 mutations are associated with chemoresistance and high risk of relapse. In patients with TP53 mutations, these alterations may lead to novel, selective vulnerabilities, creating opportunities for therapeutic targeting of TP53 mutant AML. The mutational status of TP53 therefore poses challenges and opportunities in terms of advancing effective treatment strategies in AML. An increasing armamentarium of small-molecule activators of the TP53 pathway, and a growing understanding of molecular pathways triggered by mutant TP53 have accelerated efforts aimed at targeting TP53 function in AML. In combination with standard AML chemotherapy or emerging targeted therapies, pharmacological targeting of the TP53 pathway may provide therapeutic benefit in AML.
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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.