Evidence map›Paper›PMID 22516348›Full record

ArticleMolecular cancer research : MCR2012

Somatic mutations in CCK2R alter receptor activity that promote oncogenic phenotypes.

Melinda D Willard, Mary E Lajiness, Isabella H Wulur, Bo Feng, Michelle L Swearingen, Mark T Uhlik, Kenneth W Kinzler, Victor E Velculescu, Tobias Sjöblom, Sanford D Markowitz and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2012. 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
1.4field-weighted citation impact, top 21% 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, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Expression of cholecystokinin receptors in colon cancer and the clinical correlation in Taiwan.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Gastrin receptor pharmacology.Current gastroenterology reports · 2012
    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

13 authors at 5 institutions in 1 country.

Melinda D WillardDepartment of Translational Science, Lilly Research Laboratories, Indianapolis, Indiana 46225, USA. willardme@lilly.com
Mary E Lajiness
Isabella H Wulur
Bo Feng
Michelle L Swearingen
Mark T Uhlik
Kenneth W Kinzler
Victor E Velculescu
Tobias Sjöblom
Sanford D Markowitz
Steven M Powell
Bert Vogelstein
Thomas D Barber
Howard Hughes Medical Institute · USJohns Hopkins University · USUniversity of Virginia Health System · USCase Western Reserve University · USEli Lilly (United States) · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Genes from the FAP LocusR37CA057345 · NCI · JOHNS HOPKINS UNIVERSITY · PI KINZLER, KENNETH W. · 2002 to 2016
$7.4M
Large-Scale Genetic Analyses of Human CancerR01CA121113 · NCI · JOHNS HOPKINS UNIVERSITY · PI ANAGNOSTOU, VALSAMO, VELCULESCU, VICTOR E. · 2006 to 2022
$4.3M
GENES FROM THE FAP LOCUSR01CA057345 · NCI · JOHNS HOPKINS UNIVERSITY · PI KINZLER, KENNETH W. · 1992 to 2001
$734k
Howard Hughes Medical InstituteNCI NIH HHS CA 121113NCI NIH HHS CA57345NCI NIH HHS CA62924NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA062924NCI NIH HHS R01 CA057345NCI NIH HHS R01 CA121113NCI NIH HHS R37 CA057345
6 · The paper itself

Abstract

The roles of cholecystokinin 2 receptor (CCK2R) in numerous physiologic processes in the gastrointestinal tract and central nervous system are well documented. There has been some evidence that CCK2R alterations play a role in cancers, but the functional significance of these alterations for tumorigenesis is unknown. We have identified six mutations in CCK2R among a panel of 140 colorectal cancers and 44 gastric cancers. We show that these mutations increase receptor activity, activate multiple downstream signaling pathways, increase cell migration, and promote angiogenesis. Our findings suggest that somatic mutations in CCK2R may promote tumorigenesis through deregulated receptor activity and highlight the importance of evaluating CCK2R inhibitors to block both the normal and mutant forms of the receptor.

Indexed as

MutationAnimalsCell MovementCells, CulturedCell ShapeCell Transformation, NeoplasticCoculture TechniquesColorectal NeoplasmsDNA Mutational AnalysisEndothelial CellsHEK293 CellsHumansImmunoblottingMiceMicroscopy, FluorescenceNeovascularization, PathologicReceptor, Cholecystokinin BVascular Endothelial Growth Factor A

Identifiers

PMID22516348
PMCPMC3904773
OpenAlexW2152806990

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.