Evidence map›Paper›PMID 20433877›Full record

ArticleRegulatory peptides2010

Glucose-dependent insulinotropic polypeptide stimulates the proliferation of colorectal cancer cells.

Daniel Prabakaran, Baogui Wang, Joseph D Feuerstein, Jennifer A Sinclair, Priti Bijpuria, Lisa I Jepeal, M Michael Wolfe

Open access · greenAbstract read
In one paragraph

Article in Regulatory peptides, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Incretin-Based Therapies and Cancer: What's New?Medicina (Kaunas, Lithuania) · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Cancer biology in diabetes.Journal of diabetes investigation · 2014
    Review
  14. 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

7 authors at 2 institutions in 1 country.

Daniel PrabakaranDepartment of Medicine, Boston University School of Medicine and Boston Medical Center, Boston, Massachusetts 02118, United States.
Baogui Wang
Joseph D Feuerstein
Jennifer A Sinclair
Priti Bijpuria
Lisa I Jepeal
M Michael Wolfe
Boston Medical Center · USBoston University · US

Funding

Defintion of the Physiological Properties of GIPR01DK053158 · NIDDK · BOSTON MEDICAL CENTER · PI WOLFE, MICHAEL · 1997 to 2007
$2.3M
Role of Gastrin in the Pathogenesis of Colorectal CancerR01CA118992 · NCI · BOSTON MEDICAL CENTER · PI WOLFE, M. MICHAEL · 2006 to 2008
$757k
NCI NIH HHS R01 CA118992NIDDK NIH HHS R01 DK053158NIDDK NIH HHS R01 DK53158
6 · The paper itself

Abstract

Although numerous epidemiological studies have provided convincing evidence for an increase in the prevalence of colorectal cancer (CRC) in obese individuals, the precise mechanisms involved have not been elucidated. Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal regulatory peptide whose primary physiologic role is to stimulate postprandial pancreatic insulin secretion. Like insulin, GIP has been linked to enhanced nutrient efficiency, which occurred during the course of evolution. Its expression is increased in obesity, and we thus initiated studies to examine whether GIP might contribute to the pathogenesis of obesity-related CRC. RT-PCR and Western analysis demonstrated the presence of the GIP receptor (GIPR) in several human CRC cell lines. GIP stimulated the proliferation of MC-26 cells, a mouse CRC cell line, in a concentration-dependent manner. Western analysis showed that GIP induced the activity of several downstream signaling molecules known to be involved in cellular proliferation in a concentration- and time-dependent manner. These studies indicate that the presence of GIP receptors in CRC may enable ligand binding and, in so doing, stimulate CRC cell proliferation. The overexpression of GIP, which occurs in obesity, might thereby be contributing to the enhanced rate of carcinogenesis observed in obesity.

Indexed as

AnimalsBinding SitesCell Line, TumorCell ProliferationColorectal NeoplasmsGastric Inhibitory PolypeptideHumansLigandsMiceObesityReceptors, Gastrointestinal HormoneSwineGastric Inhibitory Polypeptidegastric inhibitory polypeptide receptorLigandsReceptors, Gastrointestinal Hormone

Identifiers

PMID20433877
PMCPMC2902700
OpenAlexW2031078511

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.