Evidence map›Paper›PMID 20080664›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Stromal genes discriminate preinvasive from invasive disease, predict outcome, and highlight inflammatory pathways in digestive cancers.

Amel Saadi, Nicholas B Shannon, Pierre Lao-Sirieix, Maria O'Donovan, Elaine Walker, Nicholas J Clemons, James S Hardwick, Chunsheng Zhang, Madhumita Das, Vicki Save and 3 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
18.1field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
  2. Disintegrin and metalloproteinases (ADAMs) expression in gastroesophageal reflux disease and in esophageal adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017
    Trial
  3. Interactions between cancer-associated fibroblasts and the extracellular matrix in oesophageal cancer.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
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28 more citing papers are in PubMed but not listed here.

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 5 institutions in 2 countries.

Amel SaadiMedical Research Council Cancer Cell Unit, Hutchison Medical Research Council Research Centre, Cambridge CB22 0XZ, United Kingdom.
Nicholas B Shannon
Pierre Lao-Sirieix
Maria O'Donovan
Elaine Walker
Nicholas J Clemons
James S Hardwick
Chunsheng Zhang
Madhumita Das
Vicki Save
Marco Novelli
Frances Balkwill
Rebecca C Fitzgerald
Hutchison/MRC Research Centre · GBMedical Research Council · GBAddenbrooke's Hospital · GBUnited States Military Academy · USThe Royal Free Hospital · GB

Funding

Cancer Research UKMedical Research Council G0501974Medical Research Council MC_U105365007
6 · The paper itself

Abstract

The stromal compartment is increasingly recognized to play a role in cancer. However, its role in the transition from preinvasive to invasive disease is unknown. Most gastrointestinal tumors have clearly defined premalignant stages, and Barrett's esophagus (BE) is an ideal research model. Supervised clustering of gene expression profiles from microdissected stroma identified a gene signature that could distinguish between BE metaplasia, dysplasia, and esophageal adenocarcinoma (EAC). EAC patients overexpressing any of the five genes (TMEPAI, JMY, TSP1, FAPalpha, and BCL6) identified from this stromal signature had a significantly poorer outcome. Gene ontology analysis identified a strong inflammatory component in BE disease progression, and key pathways included cytokine-cytokine receptor interactions and TGF-beta. Increased protein levels of inflammatory-related genes significantly up-regulated in EAC compared with preinvasive stages were confirmed in the stroma of independent samples, and in vitro assays confirmed functional relevance of these genes. Gene set enrichment analysis of external datasets demonstrated that the stromal signature was also relevant in the preinvasive to invasive transition of the stomach, colon, and pancreas. These data implicate inflammatory pathways in the genesis of gastrointestinal tract cancers, which can affect prognosis.

Indexed as

AdenocarcinomaBarrett EsophagusBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCytokinesDigestive System NeoplasmsDNA-Binding ProteinsEndopeptidasesEsophageal NeoplasmsFibroblast Activation Protein AlphaGelatinasesHumansInflammationMembrane ProteinsMetaplasiaNeoplasm InvasivenessNuclear ProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBCL6 protein, humanCytokinesDNA-Binding ProteinsEndopeptidasesFibroblast Activation Protein AlphaGelatinasesJMY protein, humanMembrane ProteinsNuclear ProteinsPMEPA1 protein, humanProto-Oncogene Proteins c-bcl-6Receptors, CytokineSerine EndopeptidasesSPZ1 protein, humanTrans-Activators

Identifiers

PMID20080664
PMCPMC2836667
OpenAlexW2015300224

What OpenQuestion holds

Textmetadata
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.