Evidence map›Paper›PMID 25058882›Full record

ArticlePancreas2014

Cholecystokinin receptor antagonist halts progression of pancreatic cancer precursor lesions and fibrosis in mice.

Jill P Smith, Timothy K Cooper, Christopher O McGovern, Evan L Gilius, Qing Zhong, Jiangang Liao, Alfredo A Molinolo, J Silvio Gutkind, Gail L Matters

Open access · greenAbstract read
In one paragraph

Article in Pancreas, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  8. Implicating the cholecystokinin B receptor in liver stem cell oncogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  9. Review
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  11. Target-Specific Nanoparticle Polyplex Down-Regulates MutantInternational journal of molecular sciences · 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

9 authors at 2 institutions in 1 country.

Jill P SmithFrom the *National Institute of Diabetes and Digestive and Kidney Disease, The National Institutes of Health, Bethesda, MD; Departments of †Medicine, ‡Comparative Medicine and Pathology, §Public Health Sciences, and ∥Biochemistry and Molecular Biology, The Pennsylvania State University, College of Medicine, Hershey, PA; and ¶National Institute of Dental and Craniofacial Research, The National Institutes of Health, Bethesda, MD.
Timothy K Cooper
Christopher O McGovern
Evan L Gilius
Qing Zhong
Jiangang Liao
Alfredo A Molinolo
J Silvio Gutkind
Gail L Matters
Pennsylvania State University · USNational Institutes of Health · US

Funding

Molecular Mechanisms Of Growth Control And CarcinogenesisZIADE000551 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, JORGE SILVIO · 2009 to 2015
$11.5M
Novel Nanoparticle Therapy for Pancreatic CancerR01CA167535 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI KESTER, MARK, MATTERS, GAIL L. · 2013 to 2017
$1.6M
The Cholecystokinin-C (CCK-C) Receptor for Early Detection of Pancreatic CancerR01CA117926 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SMITH, JILL P · 2007 to 2010
$1.1M
NCI NIH HHS R01 CA117926NCI NIH HHS R01 CA167535
6 · The paper itself

Abstract

objectivesExogenous administration of cholecystokinin (CCK) induces hypertrophy and hyperplasia of the pancreas with an increase in DNA content. We hypothesized that endogenous CCK is involved in the malignant progression of pancreatic intraepithelial neoplasia (PanIN) lesions and the fibrosis associated with pancreatic cancer.

methodsThe presence of CCK receptors in early PanIN lesions was examined by immunohistochemistry in mouse and human pancreas. Pdx1-Cre/LSL-Kras transgenic mice were randomized to receive either untreated drinking water or water supplemented with a CCK receptor antagonist (proglumide, 0.1 mg/mL). Pancreas from the mice were removed and examined histologically for number and grade of PanINs after 1, 2, or 4 months of antagonist therapy.

resultsBoth CCK-A and CCK-B receptors were identified in early stage PanINs from mouse and human pancreas. The grade of PanIN lesions was reversed, and progression to advanced lesions arrested in mice treated with proglumide compared with the controls (P = 0.004). Furthermore, pancreatic fibrosis was significantly reduced in antagonist-treated animals compared with vehicle (P < 0.001).

conclusionsThese findings demonstrate that endogenous CCK is in part responsible for the development and progression of pancreatic cancer. The use of CCK receptor antagonists may have a role in cancer prophylaxis in high-risk subjects and may reduce fibrosis in the microenvironment.

Indexed as

AnimalsCarcinoma in SituCholecystokininDisease ProgressionDrug Screening Assays, AntitumorFibrosisHumansMiceMice, TransgenicPancreasPancreatic NeoplasmsPancreatitisPrecancerous ConditionsProglumideRandom AllocationReceptor, Cholecystokinin ACholecystokininProglumideReceptor, Cholecystokinin AReceptor, Cholecystokinin B

Identifiers

PMID25058882
PMCPMC4161619
OpenAlexW2000417831

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.