Evidence map›Paper›PMID 27254108›Full record

ArticleMolecular medicine (Cambridge, Mass.)2016

Low miR-187 expression promotes resistance to chemoradiation therapy in vitro and correlates with treatment failure in patients with esophageal adenocarcinoma.

Niamh Lynam-Lennon, Becky A Bibby, Ann Marie Mongan, Laure Marignol, Christian N Paxton, Katherine Geiersbach, Mary P Bronner, Jacintha O'Sullivan, John Reynolds, Stephen G Maher

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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  15. Role and mechanism of miR-187 in human cancer.American journal of translational research · 2020
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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

10 authors at 4 institutions in 3 countries.

Niamh Lynam-LennonUniversity of Dublin Trinity College, Dublin, Ireland.
Becky A BibbyUniversity of Hull, Hull, Kingston upon Hull, United Kingdom of Great Britain and Northern Ireland.
Ann Marie MonganUniversity of Dublin Trinity College, Dublin, Ireland.
Laure MarignolUniversity of Dublin Trinity College, Dublin, Ireland.
Christian N PaxtonArup Institute for Clinical and Experimental Pathology, United States.
Katherine GeiersbachUniversity of Utah and ARUP Laboratories, United States.
Mary P BronnerUniversity of Utah and ARUP Laboratories, United States.
Jacintha O'SullivanUniversity of Dublin Trinity College, Dublin, Ireland.
John ReynoldsUniversity of Dublin Trinity College, Dublin, Ireland.
Stephen G MaherUniversity of Dublin Trinity College, Dublin, Ireland.
Trinity College Dublin · IEUniversity of Hull · GBUniversity of Utah · USARUP Laboratories (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal adenocarcinoma (EAC) has a poor prognosis and is increasing in incidence in many western populations. Neoadjuvant chemoradiation therapy (CRT) followed by surgery is increasingly the standard of care for locally advanced EAC; however, resistance to treatment is a significant clinical problem. The identification of both novel biomarkers predicting response to treatment and novel therapeutic targets to enhance the efficacy of CRT are key to improving survival rates in EAC. In this study we performed global microRNA (miRNA) profiling of pre-treatment EAC biopsies and identified 67 miRNA significantly altered in patients who are resistant to CRT. One of these miRNA, miR-187, was significantly decreased in pre-treatment EAC tumors from patients having a poor response to neoadjuvant CRT, highlighting downregulation of miR-187 as a potential mechanism of treatment resistance in EAC. In vitro, miR-187 was demonstrated to play a functional role in modulating sensitivity to X-ray radiation and cisplatin in EAC and its dysregulation was demonstrated to be due to chromosomal alterations. In vitro, miR-187 altered expression of a diverse array of pathways, including the immune regulator complement component 3 (C3), serum levels of which we have previously demonstrated to predict patient response to CRT. In vivo, expression of C3 was significantly increased in tumors from patients having a poor response to CRT. This study highlights for the first time a role for miR-187 as a novel biomarker of response to CRT and a potential therapeutic target for enhancing the efficacy of CRT in EAC.

Indexed as

Drug Resistance, NeoplasmAdenocarcinomaAdultAgedCell Line, TumorChemoradiotherapyCisplatinComplement C3Down-RegulationEsophageal NeoplasmsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMicroRNAsC3 protein, humanCisplatinComplement C3MicroRNAsMIRN187 microRNA, humanChemoradiation TherapygastroenterologymicroRNAoncologyPredictive biomarker

Identifiers

PMID27254108
PMCPMC5072404
OpenAlexW2472939960

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.