Evidence map›Paper›PMID 26325105›Full record

ArticleBritish journal of cancer2015

Identification of Endoglin as an epigenetically regulated tumour-suppressor gene in lung cancer.

K O'Leary, A Shia, F Cavicchioli, V Haley, A Comino, M Merlano, F Mauri, K Walter, M Lackner, M B Wischnewsky and 3 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Endoglin and squamous cell carcinomas.Frontiers in medicine · 2023
    Article
  5. Article
  6. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Review
  9. Preclinical Efficacy of Endoglin-Targeting Antibody-Drug Conjugates for the Treatment of Ewing Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. TGFΒ-induced transcription in cancer.Seminars in cancer biology · 2017
    Review
  15. Review
  16. Review
  17. 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

13 authors at 3 institutions in 1 country.

K O'LearyBrighton and Sussex Medical School, University of Sussex, Brighton BN1 9RY, UK.
A ShiaBrighton and Sussex Medical School, University of Sussex, Brighton BN1 9RY, UK.
F CavicchioliBrighton and Sussex Medical School, University of Sussex, Brighton BN1 9RY, UK.
V HaleyBrighton and Sussex Medical School, University of Sussex, Brighton BN1 9RY, UK.
A CominoPathology Department, S. Croce General Hospital, via Coppino 26, 12100, Cuneo, Italy.
M MerlanoMedical Oncology, Oncology Department, S. Croce General Hospital, via Carle 25, 12100, Cuneo, Italy.
F MauriDepartment of Histopathology, Imperial College London, Hammersmith Campus, Du Cane Road, London, W12 0HS, UK.
K WalterOncology Biomarker Development, Genentech, Inc., 550 Grandview Boulevard, South San Francisco, CA 94080, USA.
M LacknerOncology Biomarker Development, Genentech, Inc., 550 Grandview Boulevard, South San Francisco, CA 94080, USA.
M B WischnewskyeScience Lab, Department of Biomathematics, University of Bremen, Bremen 28359, Germany.
T CrookDivision of Cancer Research, Medical Research Institute, Jacqui Wood Cancer Centre, University of Dundee, Ninewells Hospital And Medical School, Dundee DD1 9SY, UK.
C Lo NigroLaboratory of Cancer Genetics and Translational Oncology, Oncology Department, S. Croce Genreal Hospital, via Carle 25, Cuneo 12100, Italy.
P SchmidBrighton and Sussex Medical School, University of Sussex, Brighton BN1 9RY, UK.
Brighton and Sussex Medical School · GBImperial College London · GBUniversity of Sussex · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe transforming growth factor-beta (TGF- β) pathway has been implicated in proliferation, migration and invasion of various cancers. Endoglin is a TGF-β accessory receptor that modulates signalling. We identified Endoglin as an epigenetically silenced tumour-suppressor gene in lung cancer by means of a genome-wide screening approach, then sought to characterise its effect on lung cancer progression.

methodsMethylation microarray and RNA sequencing were carried out on lung cancer cell lines. Epigenetic silencing of Endoglin was confirmed by methylation and expression analyses. An expression vector and a 20-gene expression panel were used to evaluate Endoglin function. Pyrosequencing was carried out on two independent cohorts comprising 112 and 202 NSCLC cases, respectively, and the impact of Endoglin methylation on overall survival (OS) was evaluated.

resultsMethylation in the promoter region resulted in silencing of Endoglin, which could be reactivated by demethylation. Increased invasion coupled with altered EMT marker expression was observed in cell lines with an epithelial-like, but not those with a mesenchymal-like, profile when Endoglin was absent. Methylation was associated with decreased OS in stage I but not in stages II-III disease.

conclusionsWe show that Endoglin is a common target of epigenetic silencing in lung cancer. We reveal a link between Endoglin silencing and EMT progression that might be associated with decreased survival in stage I disease.

Indexed as

Gene SilencingGenes, Tumor SuppressorAntigens, CDCarcinoma, Non-Small-Cell LungCell Line, TumorDisease ProgressionDown-RegulationEndoglinGenome-Wide Association StudyHumansLung NeoplasmsMethylationPromoter Regions, GeneticProtein Array AnalysisReceptors, Cell SurfaceSequence Analysis, DNAAntigens, CDEndoglinENG protein, humanReceptors, Cell Surface

Identifiers

PMID26325105
PMCPMC4578092
OpenAlexW1220932240

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.