Evidence map›Paper›PMID 31211760›Full record

ArticleClinical and translational gastroenterology2019

Gene Expression Changes Accompanying the Duodenal Adenoma-Carcinoma Sequence in Familial Adenomatous Polyposis.

Sushrut S Thiruvengadam, Margaret OʼMalley, Lisa LaGuardia, Rocio Lopez, Zhen Wang, Bonnie L Shadrach, Yanwen Chen, Chunbiao Li, Martina L Veigl, Jill S Barnholtz-Sloan and 5 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Predicting Duodenal Cancer Risk in Patients with Familial Adenomatous Polyposis Using Machine Learning Model.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
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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

15 authors at 3 institutions in 1 country.

Sushrut S ThiruvengadamCleveland Clinic Lerner College of Medicine, Cleveland Clinic, Cleveland, Ohio, USA.
Margaret OʼMalleySanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, Ohio, USA.
Lisa LaGuardiaSanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, Ohio, USA.
Rocio LopezDepartments of Quantitative Health Science, Cleveland Clinic, Cleveland, Ohio, USA.
Zhen WangAnatomic Pathology, Cleveland Clinic, Cleveland, Ohio, USA.
Bonnie L ShadrachAnatomic Pathology, Cleveland Clinic, Cleveland, Ohio, USA.
Yanwen ChenCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, USA.
Chunbiao LiCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, USA.
Martina L VeiglCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, USA.
Jill S Barnholtz-SloanCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, USA.
Rish K PaiAnatomic Pathology, Cleveland Clinic, Cleveland, Ohio, USA.
James M ChurchSanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, Ohio, USA.
Matthew F KaladySanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, Ohio, USA.
R Matthew WalshSanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, Ohio, USA.
Carol A BurkeSanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, Ohio, USA.
Cleveland Clinic · USCase Western Reserve University · USCleveland Clinic Lerner College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDuodenal cancer in familial adenomatous polyposis (FAP) arises from adenomas. Differentially expressed genes (DEGs) in the duodenal adenoma-carcinoma pathway have been identified in murine FAP models, but similar data in patients with FAP are limited. Identifying such changes may have significance in understanding duodenal polyposis therapies and identifying cancer biomarkers. We performed a genome-wide transcriptional analysis to describe the duodenal adenoma-carcinoma sequence and determine changes distinguishing patients with FAP with and without duodenal cancer.

methodsTranscriptional profiling was performed with the Affymetrix Human Transcriptome Array 2.0 on duodenal biopsies from 12 FAP patients with duodenal cancer (FAP cases) and 12 FAP patients without cancer (FAP controls). DEGs were compared between cancer-normal, adenoma-normal, and cancer-adenoma in FAP cases and between adenomas from FAP cases and FAP controls. Significant results at P < 0.05 were filtered using fold change > 2.

resultsTwo hundred twenty-four DEGs were identified at an absolute fold change > 2. In adenoma-normal, downregulation of DEGs involved in metabolism of brush border proteins (LCT), lipids (APOB/A4), reactive oxygen species (GSTA2), and retinol (RBP2) was observed. In the cancer-adenoma comparison, upregulation of DEGs involved in cell invasion/migration (POSTN, SPP1) and downregulation of DEGs involved in Paneth differentiation (DEFA5/6) were observed. In the adenoma-adenoma comparison, downregulation of several DEGs (CLCA1, ADH1C, ANXA10) in FAP case adenomas was observed. DEGs with therapeutic potential include SPP1, which is involved in both cyclooxygenase and epidermal growth factor receptor pathways targeted by the sulindac/erlotinib combination for duodenal polyposis. DISCUSSION: We describe DEGs in the human duodenal adenoma-carcinoma sequence in FAP, which may have prognostic and therapeutic significance. Validation studies are needed to confirm these findings.

Indexed as

Gene Expression ProfilingAdenomaAdenomatous Polyposis ColiAdultAnimalsCarcinomaCell Adhesion MoleculesDuodenal NeoplasmsEpidermal Growth FactorFemaleHumansMaleMiceMiddle AgedOsteopontinCell Adhesion MoleculesEpidermal Growth FactorOsteopontinPOSTN protein, humanSPP1 protein, human

Identifiers

PMID31211760
PMCPMC6613862
OpenAlexW2953291156

What OpenQuestion holds

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LicenceCC BY
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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.