Evidence map›Paper›PMID 21630261›Full record

ArticleInternational journal of cancer2012

The neurotensin receptor-1 promotes tumor development in a sporadic but not an inflammation-associated mouse model of colon cancer.

James M Bugni, Leina Al- Rabadi, Kevin Jubbal, Iordanis Karagiannides, Gregory Lawson, Charalabos Pothoulakis

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 31% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Safety and tolerability ofEuropean journal of nuclear medicine and molecular imaging · 2021
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  12. Role of G protein-coupled receptors-microRNA interactions in gastrointestinal pathophysiology.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Review
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  20. The combined use of serum neurotensin and IL-8 as screening markers for colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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

6 authors at 3 institutions in 1 country.

James M BugniInflammatory Bowel Disease Center, Division of Digestive Diseases, David Geffen School of Medicine, Room 1240 MacDonald Research Laboratories, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Leina Al- Rabadi
Kevin Jubbal
Iordanis Karagiannides
Gregory Lawson
Charalabos Pothoulakis
University of California, Los Angeles · USIn-Q-Tel · USSouth University · US

Funding

Mechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0M
SUBSTANCE P AND INTESTINAL INFLAMMATIONR01DK047343 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 1994 to 2014
$4.2M
NIDDK NIH HHS R01 DK047343NIDDK NIH HHS R01 DK060729NIDDK NIH HHS R0-1 DK60729
6 · The paper itself

Abstract

Neurotensin receptor-1 (NTR-1) is overexpressed in colon cancers and colon cancer cell lines. Signaling through this receptor stimulates proliferation of colonocyte-derived cell lines and promotes inflammation and mucosal healing in animal models of colitis. Given the causal role of this signaling pathway in mediating colitis and the importance of inflammation in cancer development, we tested the effects of NTR-1 in mouse models of inflammation-associated and sporadic colon cancer using NTR-1-deficient (Ntsr1(-) (/-)) and wild-type (Ntsr1(+/+)) mice. In mice treated with azoxymethane (AOM) to model sporadic cancer, NTR-1 had a significant effect on tumor development with Ntsr1(+/+) mice developing over twofold more tumors than Ntsr1(-) (/-) mice (p = 0.04). There was no effect of NTR-1 on the number of aberrant crypt foci or tumor size, suggesting that NT/NTR-1 signaling promotes the conversion of precancerous cells to adenomas. Interestingly, NTR-1 status did not affect tumor development in an inflammation-associated cancer model where mice were treated with AOM followed by two cycles of 5% dextran sulfate sodium (DSS). In addition, colonic molecular and histopathologic analyses were performed shortly after a single cycle of DSS. NTR-1 status did not affect colonic myeloperoxidase activity or histopathologic scores for damage and inflammation. However, Ntsr1(-) (/-) mice were more resistant to DSS-induced mortality (p = 0.01) and had over twofold higher colonic expression levels of Il6 and Cxcl2 (p < 0.04), cytokines known to promote tumor development. These results represent the first direct demonstration that targeted disruption of the Ntsr1 gene reduces susceptibility to colon tumorigenesis.

Indexed as

Disease Models, AnimalAnimalsAzoxymethaneChemokine CXCL2ColitisColonColonic NeoplasmsDextran SulfateFemaleGene ExpressionHumansImmunohistochemistryInterleukin-6Kaplan-Meier EstimateMaleMiceAzoxymethaneChemokine CXCL2Dextran SulfateInterleukin-6neurotensin type 1 receptorPyrazolesQuinolinesReceptors, NeurotensinSR 142948Tumor Necrosis Factor-alpha

Identifiers

PMID21630261
PMCPMC3288327
OpenAlexW2043769837

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.