Evidence map›Paper›PMID 21782343›Full record

ArticlePain2011

Re-expression of the methylated EDNRB gene in oral squamous cell carcinoma attenuates cancer-induced pain.

Chi T Viet, Yi Ye, Dongmin Dang, David K Lam, Stacy Achdjian, Jianan Zhang, Brian L Schmidt

Open access · greenAbstract read
In one paragraph

Article in Pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

35 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The Epigenetics of Neuropathic Pain: A Systematic Update.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. DNMT3a methylation in neuropathic pain.Journal of pain research · 2017
    Article
  19. Article
  20. Cancer and orofacial pain.Medicina oral, patologia oral y cirugia bucal · 2016
    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

7 authors at 2 institutions in 1 country.

Chi T VietDepartment of Oral and Maxillofacial Surgery, New York University, New York, NY, USA Oral and Craniofacial Graduate Program, University of California, San Francisco, San Francisco, CA, USA Department of Oral and Maxillofacial Surgery, University of California, San Francisco, San Francisco, CA, USA Bluestone Center for Clinic Research, New York University, NY, USA.
Yi Ye
Dongmin Dang
David K Lam
Stacy Achdjian
Jianan Zhang
Brian L Schmidt
University of California, San Francisco · USNew York University · US

Funding

A Novel Gnawing Assay to Quantify Nociception in Models of Chronic Orofacial PainR21DE018561 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SCHMIDT, BRIAN L · 2007 to 2008
$422k
NIDCR NIH HHS R21 DE018561
6 · The paper itself

Abstract

Endothelin-1 is a vasoactive peptide that activates both the endothelin A (ET(A)) and endothelin B (ET(B)) receptors, and is secreted in high concentrations in many different cancer environments. Although ET(A) receptor activation has an established nociceptive effect in cancer models, the role of ET(B) receptors on cancer pain is controversial. EDNRB, the gene encoding the ET(B) receptor, has been shown to be hypermethylated and transcriptionally silenced in many different cancers. In this study we demonstrate that EDNRB is heavily methylated in human oral squamous cell carcinoma lesions, which are painful, but not methylated in human oral dysplasia lesions, which are typically not painful. ET(B) mRNA expression is reduced in the human oral squamous cell carcinoma lesions as a consequence of EDNRB hypermethylation. Using a mouse cancer pain model, we show that ET(B) receptor re-expression attenuates cancer-induced pain. These findings identify EDNRB methylation as a novel regulatory mechanism in cancer-induced pain and suggest that demethylation therapy targeted at the cancer microenvironment has the potential to thwart pain-producing mechanisms at the source, thus freeing patients of systemic analgesic toxicity.

Indexed as

AgedAged, 80 and overAnimalsCarcinoma, Squamous CellCell Line, TumorDisease Models, AnimalDNA MethylationFacial PainFemaleHumansMaleMiceMice, Inbred BALB CMiddle AgedMouth NeoplasmsReceptor, Endothelin BReceptor, Endothelin BRNA, Messenger

Identifiers

PMID21782343
PMCPMC3375027
OpenAlexW2080051564

What OpenQuestion holds

Textmetadata
LicenceTDM
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.