ArticleCell2012
The origin and evolution of mutations in acute myeloid leukemia.
Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 935 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
935 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,557 citations in OpenAlex.
- Association of clonal hematopoiesis mutations with clinical outcomes: A systematic review and meta-analysis.American journal of hematology · 2022Pooled it
- Association of Somatic Gene Mutations with Risk of Transformation into Acute Myeloid Leukemia in Patients with Myelodysplastic Syndrome: A Systematic Review and Meta-Analysis.Asian Pacific journal of cancer prevention : APJCP · 2022Pooled it
- Trial
- FLT3-ITD MRD is here to stay.Blood advances · 2026Article
- Article
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- Controversies in the Management of AML in Older Patients: A Canadian Perspective.Current oncology (Toronto, Ont.) · 2026Review
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Recrudescence of a FLT3 wild-type CMML clone after allogeneic stem cell transplant for FLT3-ITD acute myeloid leukemia.The oncologist · 2026Article
- Mutational landscape changes of AML in patients relapsing after allogeneic hematopoietic cell transplantation.Bone marrow transplantation · 2026Article
- What's hidden in plain sight? Impact of clonal hematopoiesis on the risk and progression of nonhematologic cancers.Haematologica · 2026Review
- Hematopoietic Aging and Leukemia: Mechanistic and Therapeutic Insights.International journal of molecular sciences · 2026Review
- Surface CD81 supports leukemia stem cell function and reveals a therapeutic vulnerability in acute myeloid leukemia.Signal transduction and targeted therapy · 2026Article
- The comprehensive landscape ofHaematologica · 2026Article
- Age-specific mutation profiles and their prognostic implications in pediatricHaematologica · 2026Article
- A case of intestinal tumor formation during gilteritinib therapy that resolved without discontinuing the drug.Clinical journal of gastroenterology · 2026Article
- Clonal Hematopoiesis in Cardiovascular Risk: Focus on Inflammatory Mechanisms.Journal of clinical medicine · 2026Review
- Molecular basis for the inhibition of de novo DNA methylation by TCL1A.Nature communications · 2026Article
- Modeling the evolutionary dynamics of clonal hematopoiesis.Nature genetics · 2026Review
- Reframing-renaming(?)-myelodysplastic syndromes/neoplasms and clonal hematopoiesis of indeterminate potential.Leukemia · 2026Review
875 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
54 authors at 2 institutions in 1 country.
Funding
Abstract
Most mutations in cancer genomes are thought to be acquired after the initiating event, which may cause genomic instability and drive clonal evolution. However, for acute myeloid leukemia (AML), normal karyotypes are common, and genomic instability is unusual. To better understand clonal evolution in AML, we sequenced the genomes of M3-AML samples with a known initiating event (PML-RARA) versus the genomes of normal karyotype M1-AML samples and the exomes of hematopoietic stem/progenitor cells (HSPCs) from healthy people. Collectively, the data suggest that most of the mutations found in AML genomes are actually random events that occurred in HSPCs before they acquired the initiating mutation; the mutational history of that cell is "captured" as the clone expands. In many cases, only one or two additional, cooperating mutations are needed to generate the malignant founding clone. Cells from the founding clone can acquire additional cooperating mutations, yielding subclones that can contribute to disease progression and/or relapse.
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.