ReviewBlood2020
Clonal hematopoiesis and risk for hematologic malignancy.
Review in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.
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
75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.
- Association of clonal haematopoiesis with heart failure incidence and outcomes: A systematic review and meta-analysis.European journal of heart failure · 2025Pooled it
- Epigenome-wide DNA methylation association study of CHIP provides insight into perturbed gene regulation.Nature communications · 2025Pooled it
- Trial
- Inflammation as a central driver in AML pathogenesis and therapy resistance.Science China. Life sciences · 2026Review
- Radiotherapy-Induced Side Effects: Epidemiology, Pathogenesis, Prevention and Treatments.MedComm · 2026Review
- Clonal origin tracing and integrated biomarker analysis in aHaematologica · 2026Article
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Low-FrequencyCancers · 2026Article
- Independent somatic TP53 mutations in blood and tumor mimicking Li-Fraumeni syndrome in a 94-year-old man.NPJ precision oncology · 2026Article
- Immunological consequences of chemotherapy: implications for cancer immunotherapy.Journal for immunotherapy of cancer · 2026Review
- Article
- Clonal haematopoiesis in chronic lymphocytic leukaemia: Biology, inflammaging and clinical implications in the era of targeted therapy.Clinical and translational medicine · 2026Review
- Clonal Haematopoiesis in Type 2 Diabetes: A Review of Mechanistic Links With Inflammation and Cardiovascular Disease.Diabetes/metabolism research and reviews · 2026Review
- Leucine, autoimmune diseases, and circulating mediators shape the causal landscape of lymphoid malignancies.Frontiers in immunology · 2026Article
- Real-ambient PMParticle and fibre toxicology · 2025Article
- Molecular and Clinical Insights intoInternational journal of molecular sciences · 2025Review
- Racial disparities in clonal hematopoiesis and their impact on hematologic malignancies.Journal of hematology & oncology · 2025Article
- Clonal hematopoiesis is common in bone marrow of patients with classical Hodgkin lymphoma.Haematologica · 2025Article
- Somatic mutations and the efficacy of immunosuppressive therapy in severe/very severe aplastic anemia and transfusion-dependent nonsevere aplastic anemia.Annals of hematology · 2025Article
- Clonal hematopoiesis in myeloid malignancies and solid tumors.Nature cancer · 2025Review
15 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Clonal hematopoiesis (CH) is common in older persons and is associated with an increased risk of hematologic cancer. Here, we review studies establishing an association between CH and hematopoietic malignancy, discuss features of CH that are predictive of leukemic progression, and explore the role of hematopoietic stressors in the evolution of CH to acute myeloid leukemia or myelodysplastic syndrome. CH due to point mutations or structural variants such as copy-number alterations is associated with an ∼10-fold increased risk of hematopoietic malignancy. Although the absolute risk of hematopoietic malignancy is low, certain features of CH may confer a higher risk of transformation, including the presence of TP53 or spliceosome gene mutations, a variant allele fraction >10%, the presence of multiple mutations, and altered red blood indices. CH in the setting of peripheral blood cytopenias carries a very high risk of progression to a myeloid malignancy and merits close observation. There is emerging evidence suggesting that hematopoietic stressors contribute to both the development of CH and progression to hematopoietic malignancy. Specifically, there is evidence that genotoxic stress from chemotherapy or radiation therapy, ribosome biogenesis stress, and possibly inflammation may increase the risk of transformation from CH to a myeloid malignancy. Models that incorporate features of CH along with an assessment of hematopoietic stressors may eventually help predict and prevent the development of hematopoietic malignancies.
Indexed as
Identifiers
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.