ReviewBlood2017
Dysfunctional diversity of p53 proteins in adult acute myeloid leukemia: projections on diagnostic workup and therapy.
Review in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 166 citations in OpenAlex.
- The landscape of gene co-expression modules correlating with prognostic genetic abnormalities in AML.Journal of translational medicine · 2021Trial
- Chronotherapy in Hematological Malignancies: Evaluating the Rationale and Evidence.Pharmacology research & perspectives · 2026Review
- Comment on: "Clinical interrogation ofHaematologica · 2026Article
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- Multi-omics analysis reveals LARP1 as a key integrator of translation and metabolism in AML.Oncogenesis · 2026Article
- Prognostic Landscape of TP53 Mutations in Hematologic Malignancies.Cancer research and treatment · 2026Article
- Patients with AML with WT TP53 but defective TP53-mediated apoptosis have a dismal survival.JCI insight · 2026Article
- Management of Acute Myeloid Leukemia: A Review.Cancers · 2026Review
- Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy.Blood and lymphatic cancer : targets and therapy · 2026Article
- Comparative outcome and prognostic factor analysis among MDS/AML patients with TP53 mutations, snps, and wild type.Human genomics · 2025Article
- Characterization and Clinical Implications of p53 Dysfunction in Patients With Myelodysplastic Syndromes.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Article
- Clinical interrogation ofHaematologica · 2025Article
- TP53 -Mutated Myeloid Neoplasms: 2024 Update on Diagnosis, Risk-Stratification, and Management.American journal of hematology · 2025Review
- CircTADA2A stabilizes p53 via interacting with TRIM28 and suppresses the maintenance of FLT3-ITD acute myeloid leukemia.Leukemia · 2025Article
- Article
- Immune Escape of Acute Myeloid Leukemia after Transplantation.Blood cancer discovery · 2025Review
- Iron overload mediates cytarabine resistance in AML by inhibiting the TP53 signaling pathway.Acta biochimica et biophysica Sinica · 2025Article
- 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
- Correlation of p53 oligomeric status and its subcellular localization in the presence of the AML-associated NPM mutant.PloS one · 2025Article
- Essential thrombocytosis transformed AML with TP53 mutations and its clinical implications.Discover oncology · 2024Article
46 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heterogeneous nature of acute myeloid leukemia (AML) and its poor prognosis necessitate therapeutic improvement. Current advances in AML research yield important insights regarding AML genetic, epigenetic, evolutional, and clinical diversity, all in which dysfunctional p53 plays a key role. As p53 is central to hematopoietic stem cell functions, its aberrations affect AML evolution, biology, and therapy response and usually predict poor prognosis. While in human solid tumors
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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.