ArticleNature genetics2023
Multiparameter prediction of myeloid neoplasia risk.
Article in Nature genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 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
79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.
- Pooled it
- Clonal hematopoiesis of indeterminate potential as a prognostic factor: a systematic review and meta-analysis.Blood advances · 2024Pooled it
- Derivation of a blood count-based machine learning model to prioritise sequencing for high-risk clonal haematopoiesis: a retrospective cohort study.EClinicalMedicine · 2026Article
- Cardio-Oncological Sequelae of Autologous Stem Cell Transplantation: Role of Clonal Hematopoiesis in Cardiovascular Risk.JACC. Advances · 2026Article
- Clinical management of clonal hematopoiesis.Cancer · 2026Review
- Genetic influences on haematopoiesis.Nature reviews. Genetics · 2026Review
- Statin Use and Genetically Predicted HMG-CoA Reductase Inhibition in Relation to Clonal Hematopoiesis.medRxiv : the preprint server for health sciences · 2026Article
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Article
- Clonal hematopoiesis in the setting of sickle cell disease and its relevance to curative therapies.Seminars in hematology · 2026Article
- Age distinguishes selection from causation in cancer genomes.Nature genetics · 2026Article
- Patterns and drivers of 43,617 mosaic chromosomal alterations in blood.Nature genetics · 2026Article
- Clonal haematopoiesis and cardiovascular disease, defining risk, filling gaps, and framing the future.NPJ cardiovascular health · 2026Review
- CHIP clinics: a practical overview of structure and function.Blood cancer journal · 2026Review
- Novel and emerging therapeutic strategies for clonal hematopoiesis.Haematologica · 2026Review
- Clinical decisions in clonal hematopoiesis: a contemporary review for clinicians.Haematologica · 2026Review
- Clonal hematopoiesis and its progression to myeloid neoplasms: insights into risk, biology, and therapeutic strategies.Haematologica · 2026Review
- A framework for the molecular identification of CHIP for clinical research.HGG advances · 2026Article
- Mutation-specific impairment of TET2 and DNMT3A enzymatic activity predicts clonal hematopoiesis disease risk.medRxiv : the preprint server for health sciences · 2026Article
- Harnessing genomics for early cancer detection, risk stratification and prevention.Nature genetics · 2026Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 8 institutions in 4 countries.
Funding
Abstract
The myeloid neoplasms encompass acute myeloid leukemia, myelodysplastic syndromes and myeloproliferative neoplasms. Most cases arise from the shared ancestor of clonal hematopoiesis (CH). Here we analyze data from 454,340 UK Biobank participants, of whom 1,808 developed a myeloid neoplasm 0-15 years after recruitment. We describe the differences in CH mutational landscapes and hematology/biochemistry test parameters among individuals that later develop myeloid neoplasms (pre-MN) versus controls, finding that disease-specific changes are detectable years before diagnosis. By analyzing differences between 'pre-MN' and controls, we develop and validate Cox regression models quantifying the risk of progression to each myeloid neoplasm subtype. We construct 'MN-predict', a web application that generates time-dependent predictions with the input of basic blood tests and genetic data. Our study demonstrates that many individuals that develop myeloid neoplasms can be identified years in advance and provides a framework for disease-specific prognostication that will be of substantial use to researchers and physicians.
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.