Evidence map›Paper›PMID 28320919›Full record

ArticleGenome research2017

Pan-cancer analysis distinguishes transcriptional changes of aneuploidy from proliferation.

Christopher Buccitelli, Lorena Salgueiro, Konstantina Rowald, Rocio Sotillo, Balca R Mardin, Jan O Korbel

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025
    Review
  5. Article
  6. Carcinogenesis trajectories.Frontiers in cell and developmental biology · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. E2F1 Mediates SOX17 Deficiency-Induced Pulmonary Hypertension.Hypertension (Dallas, Tex. : 1979) · 2023
    Article
  13. Article
  14. A survey of CIN measures across mechanistic models.bioRxiv : the preprint server for biology · 2023
    Article
  15. Review
  16. E2F1 Mediates SOX17 Deficiency-Induced Pulmonary Hypertension.bioRxiv : the preprint server for biology · 2023
    Article
  17. Article
  18. Article
  19. JCO precision oncology · 2022
    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

6 authors at 3 institutions in 2 countries.

Christopher BuccitelliEuropean Molecular Biology Laboratory (EMBL), Genome Biology Unit, Heidelberg 69117, Germany.
Lorena SalgueiroMolecular Thoracic Oncology, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany.
Konstantina RowaldMolecular Thoracic Oncology, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany.
Rocio SotilloMolecular Thoracic Oncology, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany.ORCID 0000-0002-0855-7917
Balca R MardinEuropean Molecular Biology Laboratory (EMBL), Genome Biology Unit, Heidelberg 69117, Germany.ORCID 0000-0002-3903-9354
Jan O KorbelEuropean Molecular Biology Laboratory (EMBL), Genome Biology Unit, Heidelberg 69117, Germany.ORCID 0000-0002-2798-3794
German Cancer Research Center · DEEuropean Molecular Biology Laboratory · DEEuropean Bioinformatics Institute · GB

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Patterns of gene expression in tumors can arise as a consequence of or result in genomic instability, characterized by the accumulation of somatic copy number alterations (SCNAs) and point mutations (PMs). Expression signatures have been widely used as markers for genomic instability, and both SCNAs and PMs could be thought to associate with distinct signatures given their different formation mechanisms. Here we test this notion by systematically investigating SCNA, PM, and transcriptome data from 2660 cancer patients representing 11 tumor types. Notably, our data indicate that similar expression signatures can be derived from correlating gene expression with either SCNA or PM load. Gene sets related to cell growth and proliferation generally associated positively, and immunoregulatory gene sets negatively, with variant burden. In-depth analyses revealed several genes whose de-regulation correlates with SCNA but not with PM burden, yielding downstream effectors of

Indexed as

AneuploidyCell ProliferationGene Expression Regulation, NeoplasticTranscriptomeCell Cycle ProteinsDNA Copy Number VariationsGenomic InstabilityHumansMutation AccumulationNeoplasmsPoint MutationCell Cycle Proteins

Identifiers

PMID28320919
PMCPMC5378169
OpenAlexW2602825449

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.