Evidence map›Paper›PMID 19627395›Full record

ArticleJournal of cellular and molecular medicine2010

CCK(2) receptor splice variant with intron 4 retention in human gastrointestinal and lung tumours.

Meike Körner, Beatrice Waser, Jean Claude Reubi, Laurence J Miller

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. [Molecular pharmaceutics · 2020
    Article
  5. Review
  6. Automated preparation of clinical grade [EJNMMI radiopharmacy and chemistry · 2019
    Article
  7. Molecular pharmaceutics · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Gastrin receptor pharmacology.Current gastroenterology reports · 2012
    Article
  16. Article
  17. Radiolabelled peptides for oncological diagnosis.European journal of nuclear medicine and molecular imaging · 2012
    Review
  18. Review
  19. Review
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

4 authors at 2 institutions in 2 countries.

Meike KörnerMayo Clinic, Cancer Center and Department of Molecular Pharmacology and Experimental Therapeutics, Scottsdale, Arizona, USA. meike.koerner@pathology.unibe.ch
Beatrice Waser
Jean Claude Reubi
Laurence J Miller
Mayo Clinic in Arizona · USUniversity of Bern · CH

Funding

Type A CCK Receptor Structure, Function and RegulationR37DK032878 · NIDDK · MAYO CLINIC COLL OF MED, MAYO CLINIC AZ · PI MILLER, LAURENCE J · 2001 to 2010
$4.5M
Type A CCK Receptor Structure, Function & RegulationR01DK032878 · NIDDK · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI MILLER, LAURENCE J · 1986 to 2014
$2.5M
NIDDK NIH HHS DK32878NIDDK NIH HHS R01 DK032878NIDDK NIH HHS R37 DK032878
6 · The paper itself

Abstract

The wild-type cholecystokinin type 2 (CCK(2)) receptor is expressed in many gastrointestinal and lung tumours. A splice variant of the CCK(2) receptor with retention of intron 4 (CCK(2)Ri4sv) showing constitutive activity associated with increased tumour growth was described in few colorectal, pancreatic and gastric cancers. Given the potential functional and clinical importance of this spliceoform, its occurrence was quantitatively characterized in a broad collection of 81 gastrointestinal and lung tumours, including insulinomas, ileal carcinoids, gastrointestinal stromal tumours (GIST), gastric, colorectal and pancreatic ductal adenocarcinomas, cholangiocellular and hepatocellular carcinomas, small cell lung cancers (SCLC), non-SCLC (nSCLC) and bronchopulmonary carcinoids, as well as 21 samples of corresponding normal tissues. These samples were assessed for transcript expression of total CCK(2) receptor, wild-type CCK(2) receptor and CCK(2)Ri4sv with end-point and real-time RT-PCR, and for total CCK(2) receptor protein expression on the basis of receptor binding with in vitro receptor autoradiography. Wild-type CCK(2) receptor transcripts were found in the vast majority of tumours and normal tissues. CCK(2)Ri4sv mRNA expression was present predominantly in insulinomas (incidence 100%), GIST (100%) and SCLC (67%), but rarely in pancreatic, colorectal and gastric carcinomas and nSCLC. It was not found in wild-type CCK(2) receptor negative tumours or any normal tissues tested. CCK(2)Ri4sv transcript levels in individual tumours were low, ranging from 0.02% to 0.14% of total CCK(2) receptor transcripts. In conclusion, the CCK(2)Ri4sv is a marker of specific gastrointestinal and lung tumours. With its high selectivity for and high incidence in SCLC and GIST, it may represent an attractive clinical target.

Indexed as

Alternative SplicingAutoradiographyBinding SitesGastrointestinal NeoplasmsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntronsLung NeoplasmsReceptor, Cholecystokinin BReference StandardsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSensitivity and SpecificityReceptor, Cholecystokinin BRNA, Messenger

Identifiers

PMID19627395
PMCPMC2888751
OpenAlexW2071188859

What OpenQuestion holds

Textmetadata
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.