Evidence map›Paper›PMID 26171582›Full record

ArticleGenes, chromosomes & cancer2015

Gene expression in colon cancer: A focus on tumor site and molecular phenotype.

Martha L Slattery, Daniel F Pellatt, Lila E Mullany, Roger K Wolff, Jennifer S Herrick

Open access · greenAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

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  7. Utility ofGlobal medical genetics · 2020
    Review
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  16. Dysregulated genes and miRNAs in the apoptosis pathway in colorectal cancer patients.Apoptosis : an international journal on programmed cell death · 2018
    Article
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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

5 authors at 1 institution in 1 country.

Martha L SlatteryDepartment of Internal Medicine, University of Utah, 383 Colorow, Salt Lake City, Utah, 84117.
Daniel F PellattDepartment of Internal Medicine, University of Utah, 383 Colorow, Salt Lake City, Utah, 84117.
Lila E MullanyDepartment of Internal Medicine, University of Utah, 383 Colorow, Salt Lake City, Utah, 84117.
Roger K WolffDepartment of Internal Medicine, University of Utah, 383 Colorow, Salt Lake City, Utah, 84117.
Jennifer S HerrickDepartment of Internal Medicine, University of Utah, 383 Colorow, Salt Lake City, Utah, 84117.
University of Utah · US

Funding

DIET, ACTIVITY &REPRODUCTION--RISKS FOR RECTAL CANCERR01CA048998 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA L · 1991 to 2012
$7.9M
miRNA and colorectal cancer: associations with tumor phenotype and survivalR01CA163683 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA L · 2012 to 2017
$6.5M
DIET, ACTIVITY &REPRODUCTION--RISKS FOR RECTAL CANCERU01CA048998 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA OR MARTY L · 1997 to 1999
–
NCI NIH HHS CA48998NCI NIH HHS R01 CA048998NCI NIH HHS R01 CA163683NCI NIH HHS U01 CA048998
6 · The paper itself

Abstract

Hundreds to thousands of genes are differentially expressed in tumors when compared to nontumor colonic tissue samples. We evaluated gene expression patterns to better understand differences in colon cancer by tumor site and tumor molecular phenotype. We analyzed RNA-seq data from tumor/normal paired samples from 175 colon cancer patients. We implemented a cross validation strategy with nonparametric tests to identify genes which displayed varying expression characteristics related to paired tumor/nontumor tissue across proximal and distal colon sites and by tumor molecular phenotypes, that is, TP53, KRAS, CpG Island Methylator Phenotype (CIMP), and microsatellite instability (MSI). We used Ingenuity Pathway Analysis (IPA) to determine networks associated with deregulated genes in our data. Genes showed significant differences in expression characteristics at the 0.01 level in both validation groups between tumor subsite (116 genes), CIMP high versus CIMP low (79 genes), MSI versus microsatellite stable (MSS) (49 genes), TP53-mutated versus not mutated (17genes), and KRAS-mutated versus not mutated (1 gene). Deregulated genes for CIMP high and MSI tumors were often down-regulated. In contrast to CIMP high and MSI tumors, genes that were deregulated in TP53 were likely to be up-regulated. ERK1, WNT, growth factors and inflammation-related factors were focal points of both CIMP and MSI IPA networks. The MUC family of genes was up-regulated MSI networks. Numerous genes showed differences in expression between proximal and distal tumors, nontumor proximal and distal tissue, and tumor molecular phenotype. Deregulated mucin genes appear to play an important role in MSI tumors.

Indexed as

TranscriptomeAdenocarcinomaAgedCase-Control StudiesColonColonic NeoplasmsCpG IslandsDNA MethylationFemaleHumansMaleMicrosatellite InstabilityMiddle AgedSequence Analysis, RNA

Identifiers

PMID26171582
PMCPMC5998821
OpenAlexW1756055907

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.