Evidence map›Paper›PMID 31911629›Full record

ArticleNature communications2020

Single-cell analysis based dissection of clonality in myelofibrosis.

Elena Mylonas, Kenichi Yoshida, Mareike Frick, Kaja Hoyer, Friederike Christen, Jaspal Kaeda, Matthias Obenaus, Daniel Noerenberg, Cornelius Hennch, Willy Chan and 12 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Molecular profiling in MPN: who should have it and why?Hematology. American Society of Hematology. Education Program · 2024
    Review
  9. Investigational drugs in early phase trials for myelofibrosis.Expert opinion on investigational drugs · 2024
    Review
  10. JAK Inhibitors for Myelofibrosis: Strengths and Limitations.Current hematologic malignancy reports · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Myeloproliferative Neoplasms: Contemporary Review and Molecular Landscape.International journal of molecular sciences · 2023
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 7 institutions in 6 countries.

Elena MylonasCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.ORCID http://orcid.org/0000-0001-6831-969X
Kenichi YoshidaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID http://orcid.org/0000-0003-4612-2778
Mareike FrickCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Kaja HoyerCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Friederike ChristenCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Jaspal KaedaCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Matthias ObenausCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Daniel NoerenbergCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Cornelius HennchCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.ORCID http://orcid.org/0000-0003-4104-5531
Willy ChanCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Yotaro OchiDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yuichi ShiraishiLaboratory of Sequence Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yusuke ShiozawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Thorsten ZenzDepartment of Medical Oncology and Hematology, University Hospital Zurich / University of Zurich, Zurich, Switzerland.
Christopher C OakesDivision of Hematology, Department of Internal Medicine, The Ohio State University, Columbus, OH, USA.
Birgit SawitzkiCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute for Medical Immunology, Berlin, Germany.
Michaela SchwarzCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Lars BullingerCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Philipp le CoutreCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany.
Matthew J J Rose-ZerilliCancer Sciences, Faculty of Medicine, University of Southampton, Southampton, UK.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Frederik DammCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Hematology, Oncology, and Tumor Immunology, Berlin, Germany. frederik.damm@charite.de.
Humboldt-Universität zu Berlin · DEKyoto University · JPGerman Cancer Research Center · DEThe Ohio State University · USThe University of Tokyo · JPUniversity of Southampton · GBUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer development is an evolutionary genomic process with parallels to Darwinian selection. It requires acquisition of multiple somatic mutations that collectively cause a malignant phenotype and continuous clonal evolution is often linked to tumor progression. Here, we show the clonal evolution structure in 15 myelofibrosis (MF) patients while receiving treatment with JAK inhibitors (mean follow-up 3.9 years). Whole-exome sequencing at multiple time points reveal acquisition of somatic mutations and copy number aberrations over time. While JAK inhibition therapy does not seem to create a clear evolutionary bottleneck, we observe a more complex clonal architecture over time, and appearance of unrelated clones. Disease progression associates with increased genetic heterogeneity and gain of RAS/RTK pathway mutations. Clonal diversity results in clone-specific expansion within different myeloid cell lineages. Single-cell genotyping of circulating CD34 + progenitor cells allows the reconstruction of MF phylogeny demonstrating loss of heterozygosity and parallel evolution as recurrent events.

Indexed as

Clonal EvolutionAgedExomeFemaleFollow-Up StudiesGenetic HeterogeneityHumansMaleMiddle AgedMutationOncogene Protein p21(ras)Primary MyelofibrosisProspective StudiesSingle-Cell AnalysisStem CellsOncogene Protein p21(ras)

Identifiers

PMID31911629
PMCPMC6946829
OpenAlexW2999328297

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.