ArticleLeukemia2015
Clonal evolution revealed by whole genome sequencing in a case of primary myelofibrosis transformed to secondary acute myeloid leukemia.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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
29 citing papers in PubMed.
- Correlation of mutation profile and response in patients with myelofibrosis treated with ruxolitinib.Blood · 2015Trial
- Case Report: The diagnostic and therapeutic crossroads: when myelofibrosis transforms into mixed phenotype acute leukemia.Frontiers in oncology · 2026Article
- Article
- Phenotypically-defined stages of leukemia arrest predict main driver mutations subgroups, and outcome in acute myeloid leukemia.Blood cancer journal · 2022Article
- Article
- Coexistence of Primary Myelofibrosis and Paroxysmal Nocturnal Hemoglobinuria Clone withDiagnostics (Basel, Switzerland) · 2021Article
- Molecular pathogenesis of the myeloproliferative neoplasms.Journal of hematology & oncology · 2021Review
- New progress in the study of germline susceptibility genes of myeloid neoplasms.Oncology letters · 2021Review
- Review
- Review
- Myelofibrosis in 2019: moving beyond JAK2 inhibition.Blood cancer journal · 2019Review
- Identification of functionally primitive and immunophenotypically distinct subpopulations in secondary acute myeloid leukemia by mass cytometry.Cytometry. Part B, Clinical cytometry · 2019Article
- Clonal evolution revealed by next-generation sequencing in a long-term follow-up patient with hypereosinophilia.Leukemia research reports · 2019Article
- Article
- Genetic Alterations in Essential Thrombocythemia Progression to Acute Myeloid Leukemia: A Case Series and Review of the Literature.Frontiers in oncology · 2018Article
- Mass cytometry analysis reveals hyperactive NF Kappa B signaling in myelofibrosis and secondary acute myeloid leukemia.Leukemia · 2017Article
- Article
- Recurrent somatic JAK-STAT pathway variants within a RUNX1-mutated pedigree.European journal of human genetics : EJHG · 2017Article
- The distinct biological implications of Asxl1 mutation and its roles in leukemogenesis revealed by a knock-in mouse model.Journal of hematology & oncology · 2017Article
- Changes in allele frequencies ofHaematologica · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Clonal architecture in myeloproliferative neoplasms (MPNs) is poorly understood. Here we report genomic analyses of a patient with primary myelofibrosis (PMF) transformed to secondary acute myeloid leukemia (sAML). Whole genome sequencing (WGS) was performed on PMF and sAML diagnosis samples, with skin included as a germline surrogate. Deep sequencing validation was performed on the WGS samples and an additional sample obtained during sAML remission/relapsed PMF. Clustering analysis of 649 validated somatic single-nucleotide variants revealed four distinct clonal groups, each including putative driver mutations. The first group (including JAK2 and U2AF1), representing the founding clone, included mutations with high frequency at all three disease stages. The second clonal group (including MYB) was present only in PMF, suggesting the presence of a clone that was dispensable for transformation. The third group (including ASXL1) contained mutations with low frequency in PMF and high frequency in subsequent samples, indicating evolution of the dominant clone with disease progression. The fourth clonal group (including IDH1 and RUNX1) was acquired at sAML transformation and was predominantly absent at sAML remission/relapsed PMF. Taken together, these findings illustrate the complex clonal dynamics associated with disease evolution in MPNs and sAML.
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.