Evidence map›Paper›PMID 25768946›Full record

ArticlePLoS genetics2015

Clonality and evolutionary history of rhabdomyosarcoma.

Li Chen, Jack F Shern, Jun S Wei, Marielle E Yohe, Young K Song, Laura Hurd, Hongling Liao, Daniel Catchpoole, Stephen X Skapek, Frederic G Barr and 2 more

Abstract read
In one paragraph

Article in PLoS genetics, 2015. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
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  8. Review
  9. Epigenetic determinants of fusion-driven sarcomas: paradigms and challenges.Frontiers in cell and developmental biology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  18. [Genomic classification and survival of patients with rhabdomyosarcoma: a report from an international consortium].Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2022
    Article
  19. Article
  20. Review
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

12 authors.

Li ChenGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Jack F ShernGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America; Pediatric Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland, United States of America.
Jun S WeiGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Marielle E YoheGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America; Pediatric Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland, United States of America.
Young K SongGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Laura HurdGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Hongling LiaoGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Daniel CatchpooleBiospecimens Research and Tumour Bank, The Kids Research Institute, The Children's Hospital at Westmead, Westmead, New South Wales, Australia.
Stephen X SkapekDepartment of Pediatrics, Division of Pediatric Hematology/Oncology, UT Southwestern Medical Center, Dallas, Texas, United States of America.
Frederic G BarrLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Douglas S HawkinsDepartment of Pediatrics, Seattle Children's Hospital, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Javed KhanGenetics Branch, Oncogenomics Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America; Pediatric Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland, United States of America.

Funding

LAB RESEARCH TRAINING IN PEDIATRIC ONCOLOGY-HEMATOLOGYT32CA060441 · NCI · JOHNS HOPKINS UNIVERSITY · PI ALAN D FRIEDMAN · 1993 to 2026
$14.9M
Therapy Resistance Mechanisms for CancerZIABC010998 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KHAN, JAVED · 2009 to 2025
$14.5M
BIOINFORMATICS: SYSTEMS BIOLOGY OF PEDIATRIC CANCERSZIABC011002 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KHAN, JAVED · 2009 to 2025
$9.3M
Studies of gene fusions in rhabdomyosarcomaZIABC011387 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BARR, FREDERIC · 2011 to 2025
$9.1M
Genomic characterization and development of therapies for RhabdomyosarcomaZIABC011722 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SHERN, JOHN · 2016 to 2025
$6.8M
Intramural NIH HHSNCI NIH HHS T32 CA060441
6 · The paper itself

Abstract

To infer the subclonality of rhabdomyosarcoma (RMS) and predict the temporal order of genetic events for the tumorigenic process, and to identify novel drivers, we applied a systematic method that takes into account germline and somatic alterations in 44 tumor-normal RMS pairs using deep whole-genome sequencing. Intriguingly, we find that loss of heterozygosity of 11p15.5 and mutations in RAS pathway genes occur early in the evolutionary history of the PAX-fusion-negative-RMS (PFN-RMS) subtype. We discover several early mutations in non-RAS mutated samples and predict them to be drivers in PFN-RMS including recurrent mutation of PKN1. In contrast, we find that PAX-fusion-positive (PFP) subtype tumors have undergone whole-genome duplication in the late stage of cancer evolutionary history and have acquired fewer mutations and subclones than PFN-RMS. Moreover we predict that the PAX3-FOXO1 fusion event occurs earlier than the whole genome duplication. Our findings provide information critical to the understanding of tumorigenesis of RMS.

Indexed as

Genome, HumanSequence Analysis, DNAAdolescentChildChild, PreschoolChromosomes, Human, Pair 11Genome-Wide Association StudyHumansInfantLoss of HeterozygosityOncogene Proteins, FusionPaired Box Transcription FactorsRhabdomyosarcomaOncogene Proteins, FusionPaired Box Transcription FactorsPAX3-FOXO1A fusion protein, human

Identifiers

PMID25768946
PMCPMC4358975

What Socratic holds

Textmetadata
LicenceCC0
Read underepoch 390

Registered trials

None linked

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 Socratic graph.