Evidence map›Paper›PMID 29765148›Full record

ArticleBritish journal of cancer2018

Cancer subtype identification using somatic mutation data.

Marieke Lydia Kuijjer, Joseph Nathaniel Paulson, Peter Salzman, Wei Ding, John Quackenbush

Abstract read
In one paragraph

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

5 authors.

Marieke Lydia KuijjerDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA. mkuijjer@jimmy.harvard.edu.ORCID http://orcid.org/0000-0001-6280-3130
Joseph Nathaniel PaulsonDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA.
Peter SalzmanBristol-Myers Squibb, Devens, MA, USA.
Wei DingDepartment of Computer Science, University of Massachusetts, Boston, MA, USA.
John QuackenbushDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA.

Funding

Statistical Methods for Analysis of Massive Genetic and Genomic Data in Cancer ResearchR35CA197449 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI XIHONG LIN · 2015 to 2026
$10.9M
MeV: Software for Next Generation Genomic Data AnalysisU01CA151118 · NCI · DANA-FARBER CANCER INST · PI QUACKENBUSH, JOHN · 2011 to 2015
$2.9M
NCI NIH HHS R35 CA197449NCI NIH HHS U01 CA151118
6 · The paper itself

Abstract

backgroundWith the onset of next-generation sequencing technologies, we have made great progress in identifying recurrent mutational drivers of cancer. As cancer tissues are now frequently screened for specific sets of mutations, a large amount of samples has become available for analysis. Classification of patients with similar mutation profiles may help identifying subgroups of patients who might benefit from specific types of treatment. However, classification based on somatic mutations is challenging due to the sparseness and heterogeneity of the data.

methodsHere we describe a new method to de-sparsify somatic mutation data using biological pathways. We applied this method to 23 cancer types from The Cancer Genome Atlas, including samples from 5805 primary tumours.

resultsWe show that, for most cancer types, de-sparsified mutation data associate with phenotypic data. We identify poor prognostic subtypes in three cancer types, which are associated with mutations in signal transduction pathways for which targeted treatment options are available. We identify subtype-drug associations for 14 additional subtypes. Finally, we perform a pan-cancer subtyping analysis and identify nine pan-cancer subtypes, which associate with mutations in four overarching sets of biological pathways.

conclusionsThis study is an important step toward understanding mutational patterns in cancer.

Indexed as

MutationBiomarkers, TumorComputational BiologyDatabases, GeneticData CurationFemaleGene Regulatory NetworksHumansNeoplasmsPrincipal Component AnalysisPrognosisBiomarkers, Tumor

Identifiers

PMID29765148
PMCPMC5988673

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.