Evidence map›Paper›PMID 28295365›Full record

ArticleThe Journal of pathology2017

Comparative transcriptome analysis of isogenic cell line models and primary cancers links capicua (CIC) loss to activation of the MAPK signalling cascade.

Veronique G LeBlanc, Marlo Firme, Jungeun Song, Susanna Y Chan, Min Hye Lee, Stephen Yip, Suganthi Chittaranjan, Marco A Marra

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Genetic mechanisms of resistance to targeted KRAS inhibition.bioRxiv : the preprint server for biology · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. ThebioRxiv : the preprint server for biology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. TheeLife · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Capicua in Human Cancer.Trends in cancer · 2021
    Review
  19. 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

8 authors at 2 institutions in 1 country.

Veronique G LeBlancCanada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada.
Marlo FirmeCanada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada.
Jungeun SongCanada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada.
Susanna Y ChanCanada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada.
Min Hye LeeCanada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada.
Stephen YipDepartment of Pathology and Laboratory Medicine, University of British Columbia, BC, Canada.
Suganthi ChittaranjanCanada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada.
Marco A MarraCanada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, Canada.ORCID 0000-0001-7146-7175
BC Cancer Agency · CAUniversity of British Columbia · CA

Funding

CIHR
6 · The paper itself

Abstract

CIC encodes a transcriptional repressor, capicua (CIC), whose disrupted activity appears to be involved in several cancer types, including type I low-grade gliomas (LGGs) and stomach adenocarcinomas (STADs). To explore human CIC's transcriptional network in an isogenic background, we developed novel isogenic CIC knockout cell lines as model systems, and used these in transcriptome analyses to study the consequences of CIC loss. We also compared our results with analyses of transcriptome data from TCGA for type I LGGs and STADs. We identified 39 candidate targets of CIC transcriptional regulation, and confirmed seven of these as direct targets. We showed that, although many CIC targets appear to be context-specific, the effects of CIC loss converge on the dysregulation of similar biological processes in different cancer types. For example, we found that CIC deficiency was associated with disruptions in the expression of genes involved in cell-cell adhesion, and in the development of several cell and tissue types. We also showed that loss of CIC leads to overexpression of downstream members of the mitogen-activated protein kinase (MAPK) signalling cascade, indicating that CIC deficiency may present a novel mechanism for activation of this oncogenic pathway. © 2017 The Authors. Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Indexed as

TranscriptomeAdenocarcinomaCell Line, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockout TechniquesGliomaHumansMaleMAP Kinase Signaling SystemMitogen-Activated Protein KinasesOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticRepressor ProteinsStomach NeoplasmsCIC protein, humanMitogen-Activated Protein KinasesRepressor ProteinscapicuagliomaMAPK signallingstomach adenocarcinoma

Identifiers

PMID28295365
PMCPMC5485162
OpenAlexW2596568799

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.