ReviewCurrent opinion in hematology2019
p53 involvement in clonal hematopoiesis of indeterminate potential.
Review in Current opinion in hematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Measurable residual disease testing in acute myeloid leukemia: current state, foundational models, and tools for future development.Cancer metastasis reviews · 2026Review
- Germline pathogenic variants detected by GenMineTOP: insight from a nationwide tumor/normal paired comprehensive genomic profiling test, in Japan.Journal of human genetics · 2026Article
- Molecular and Clinical Insights intoInternational journal of molecular sciences · 2025Review
- Review
- Concordance between cancer gene alterations in tumor and circulating tumor DNA correlates with poor survival in a real-world precision-medicine population.Molecular oncology · 2023Article
- Mutation Analysis of Pancreatic Juice and Plasma for the Detection of Pancreatic Cancer.International journal of molecular sciences · 2023Article
- TP53 Alterations in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Biomedicines · 2023Review
- A sheep in wolf's clothing? Wild-type P53 disguises as mutant to promote leukemogenesis.Haematologica · 2022Article
- Clonal hematopoiesis: Mutation-specific adaptation to environmental change.Cell stem cell · 2022Review
- Overview of the Clinical Features of Li-Fraumeni Syndrome and the Current European ERN GENTURIS Guideline.Geburtshilfe und Frauenheilkunde · 2022Article
- p53-dependent induction of P2X7 on hematopoietic stem and progenitor cells regulates hematopoietic response to genotoxic stress.Cell death & disease · 2021Article
- Clonal haematopoiesis of indeterminate potential: intersections between inflammation, vascular disease and heart failure.Clinical science (London, England : 1979) · 2021Review
- Circulating Tumor DNA Profiling From Breast Cancer Screening Through to Metastatic Disease.JCO precision oncology · 2021Article
- New surveillance guidelines for Li-Fraumeni and hereditary TP53 related cancer syndrome: implications for germline TP53 testing in breast cancer.Familial cancer · 2021Article
- GermlineCancers · 2020Review
- Transient expansion of TP53 mutated clones in polycythemia vera patients treated with idasanutlin.Blood advances · 2020Article
- AML chemoresistance: The role of mutant TP53 subclonal expansion and therapy strategy.Experimental hematology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewClonal hematopoiesis of indeterminate potential (CHIP) increases with age and occurs when a single mutant hematopoietic stem cell (HSC) contributes to a significant clonal proportion of mature blood lineages. Somatic mutations in the TP53 gene, which encodes the tumor suppressor protein p53, rank in the top five among genes that were mutated in CHIP. This review focuses on mechanisms by which mutant p53 promotes CHIP progression and drives the pathogenesis of hematological malignancies, including myelodysplastic syndromes, and acute myeloid leukemia. RECENT
findingsTP53 was frequently mutated in individuals with CHIP. Although clinical studies suggest that expansion of HSCs with TP53 mutations predisposes the elderly to hematological neoplasms, there is a significant gap in knowledge regarding the mechanisms by which TP53 mutations promote HSC expansion. Recent findings suggest that several cellular stressors, including hematopoietic transplantation, genotoxic stress, and inflammation, promote the expansion of HSCs with TP53 mutations. Further, TP53 mutations identified in CHIP cooperate with genetic and/or epigenetic changes in leukemogenesis. SUMMARY: TP53 mutations identified in CHIP are associated with increased risks of de novo and therapy-related hematological neoplasms. Thus, targeting mutant p53 and related pathways holds great potential in preventing CHIP progression and treating hematological malignancies.
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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.