Evidence map›Paper›PMID 24177718›Full record

ArticleBioinformatics (Oxford, England)2014

EXPANDS: expanding ploidy and allele frequency on nested subpopulations.

Noemi Andor, Julie V Harness, Sabine Müller, Hans W Mewes, Claudia Petritsch

Abstract read
In one paragraph

Article in Bioinformatics (Oxford, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing 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

91 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
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  5. Cell lineage tracing: Methods, applications, and challenges.Quantitative biology (Beijing, China) · 2025
    Review
  6. Article
  7. Review
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  9. Article
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  16. Intratumor Heterogeneity and Antitumor Immunity Shape One Another Bidirectionally.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Review
  17. Accurate Identification of Subclones in Tumor Genomes.Molecular biology and evolution · 2022
    Article
  18. Article
  19. Article
  20. Article

31 more citing papers are in PubMed but not listed here.

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

5 authors.

Noemi AndorDepartment of Neurological Surgery, University of California San Francisco, San Francisco, CA 94143, USA, Institute of Bioinformatics and Systems Biology, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany, Brain Tumor Research Center, University of California San Francisco, San Francisco, CA 94158, USA, Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA, Department of Pediatrics, University of California San Francisco, San Francisco, CA 94143, USA, Chair of Genome Oriented Bioinformatics, Center of Life and Food Science, Freising-Weihenstephan, Technische Universität München, 80333, Munich, Germany, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158 and Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco, San Francisco, CA 94143, USA.
Julie V Harness
Sabine Müller
Hans W Mewes
Claudia Petritsch

Funding

Training Program in Translational Brain Tumor ResearchT32CA151022 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joseph F Costello · 2010 to 2026
$6.6M
BRAF Mutation in Malignant Astrocytoma Origin, Evolution, and Response to TherapyR01NS080619 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAMES, CHARLES DAVID, PETRITSCH, CLAUDIA KATHARINA · 2012 to 2016
$1.8M
A causal role for asymmetric cell division defects in glioma initiationR01CA164746 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PETRITSCH, CLAUDIA KATHARINA · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA164746NCI NIH HHS R01CA164746NCI NIH HHS T32 CA151022NINDS NIH HHS R01 NS080619NINDS NIH HHS R01NS080619
6 · The paper itself

Abstract

motivationSeveral cancer types consist of multiple genetically and phenotypically distinct subpopulations. The underlying mechanism for this intra-tumoral heterogeneity can be explained by the clonal evolution model, whereby growth advantageous mutations cause the expansion of cancer cell subclones. The recurrent phenotype of many cancers may be a consequence of these coexisting subpopulations responding unequally to therapies. Methods to computationally infer tumor evolution and subpopulation diversity are emerging and they hold the promise to improve the understanding of genetic and molecular determinants of recurrence.

resultsTo address cellular subpopulation dynamics within human tumors, we developed a bioinformatic method, EXPANDS. It estimates the proportion of cells harboring specific mutations in a tumor. By modeling cellular frequencies as probability distributions, EXPANDS predicts mutations that accumulate in a cell before its clonal expansion. We assessed the performance of EXPANDS on one whole genome sequenced breast cancer and performed SP analyses on 118 glioblastoma multiforme samples obtained from TCGA. Our results inform about the extent of subclonal diversity in primary glioblastoma, subpopulation dynamics during recurrence and provide a set of candidate genes mutated in the most well-adapted subpopulations. In summary, EXPANDS predicts tumor purity and subclonal composition from sequencing data. AVAILABILITY AND IMPLEMENTATION: EXPANDS is available for download at http://code.google.com/p/expands (matlab version--used in this manuscript) and http://cran.r-project.org/web/packages/expands (R version).

Indexed as

Gene FrequencyPloidiesGlioblastomaHumansMutationNeoplasmsProbabilityRecurrence

Identifiers

PMID24177718
PMCPMC3866558

What OpenQuestion holds

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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.