ArticleBlood2022
TP53 copy number and protein expression inform mutation status across risk categories in acute myeloid leukemia.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Contemporary Approach to the Diagnosis and Classification of Myelodysplastic Neoplasms/Syndromes-Recommendations From the International Consortium for Myelodysplastic Neoplasms/Syndromes (MDS [icMDS]).Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024Guideline
- p53 Immunohistochemistry Is a Reliable Method for Assessing TP53 Allelic and Functional Status in TP53-Mutated Cases.American journal of hematology · 2026Article
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- A novel prognostic biomarker combiningOncology letters · 2026Article
- Identification of two novel TP53 mutations in secondary acute myeloid leukemia following multiple myeloma: a case report.Blood science (Baltimore, Md.) · 2026Article
- Wild-Type p53 Protein Enhances APR-246-Induced Cytotoxicity in Acute Myeloid Leukemia and Normal Hematopoietic Stem/Progenitor Cells.International journal of molecular sciences · 2026Article
- REST-driven upregulation of SFXN3 promotes AML progression via Wnt/β-catenin activation and confers decitabine resistance.Translational oncology · 2026Article
- Construction of a predictive model based on the risk of relapse after cytarabine consolidation therapy in acute myeloid leukemia patients.The oncologist · 2026Article
- The prognostic impact of myeloid co-mutation burden in TP53-mutated AML/MDS after allogeneic stem cell transplantation: a multicenter retrospective analysis.Annals of hematology · 2026Article
- Wild-type p53 overexpression inHaematologica · 2026Article
- CharacterizingCancers · 2026Article
- Coagulation activation is associated with genomic-instability-related features in TP53-mutated AML and MDS: routine laboratory patterns beyond classical disseminated intravascular coagulation.Frontiers in cell and developmental biology · 2026Article
- Interpretation of p53 immunohistochemical stain of TP53-mutated myeloid neoplasms.Frontiers in oncology · 2026Article
- Application of artificial intelligence in laboratory hematology: Advances, challenges, and prospects.Acta pharmaceutica Sinica. B · 2025Review
- Review
- CDK4/6 Inhibitors in Breast Cancer-Who Should Receive Them?International journal of molecular sciences · 2025Review
- Correlation between TP53 mutational status and digital quantification of p53 immunohistochemistry in mantle cell lymphoma.Virchows Archiv : an international journal of pathology · 2025Article
- Article
- Decision level scheme for fusing multiomics and histology slide images using deep neural network for tumor prognosis prediction.Scientific reports · 2025Article
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutant TP53 is an adverse risk factor in acute myeloid leukemia (AML), but large-scale integrated genomic-proteomic analyses of TP53 alterations in patients with AML remain limited. We analyzed TP53 mutational status, copy number (CN), and protein expression data in AML (N = 528) and provide a compilation of mutation sites and types across disease subgroups among treated and untreated patients. Our analysis shows differential hotspots in subsets of AML and uncovers novel pathogenic variants involving TP53 splice sites. In addition, we identified TP53 CN loss in 70.2% of TP53-mutated AML cases, which have more deleterious TP53 mutations, as well as copy neutral loss of heterozygosity in 5/32 (15.6%) AML patients who had intact TP53 CN. Importantly, we demonstrate that mutant p53 protein expression patterns by immunohistochemistry evaluated using digital image-assisted analysis provide a robust readout that integrates TP53 mutation and allelic states in patients with AML. Expression of p53 by immunohistochemistry informed mutation status irrespective of TP53 CN status. Genomic analysis of comutations in TP53-mutant AML shows a muted landscape encompassing primarily mutations in genes involved in epigenetic regulation (DNMT3A and TET2), RAS/MAPK signaling (NF1, KRAS/NRAS, PTPN11), and RNA splicing (SRSF2). In summary, our data provide a rationale to refine risk stratification of patients with AML on the basis of integrated molecular and protein-level TP53 analyses.
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