Evidence map›Paper›PMID 20569440›Full record

ArticleBMC cancer2010

Alterations in LMTK2, MSMB and HNF1B gene expression are associated with the development of prostate cancer.

Lorna W Harries, John R B Perry, Paul McCullagh, Malcolm Crundwell

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Lemur Tyrosine Kinases and Prostate Cancer: A Literature Review.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Lorna W HarriesInstitute of Biomedical and Clinical Sciences, Peninsula NIHR Clinical Research Facility, University of Exeter, Peninsula Medical School, Exeter, Devon, UK. L.W.Harries@exeter.ac.uk
John R B Perry
Paul McCullagh
Malcolm Crundwell
Royal Devon & Exeter NHS Foundation Trust · GBUniversity of Exeter · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenome wide association studies (GWAS) have identified several genetic variants that are associated with prostate cancer. Most of these variants, like other GWAS association signals, are located in non-coding regions of potential candidate genes, and thus could act at the level of the mRNA transcript.

methodsWe measured the expression and isoform usage of seven prostate cancer candidate genes in benign and malignant prostate by real-time PCR, and correlated these factors with cancer status and genotype at the GWAS risk variants.

resultsWe determined that levels of LMTK2 transcripts in prostate adenocarcinomas were only 32% of those in benign tissues (p = 3.2 x 10(-7)), and that an independent effect of genotype at variant rs6465657 on LMTK2 expression in benign (n = 39) and malignant tissues (n = 21) was also evident (P = 0.002). We also identified that whilst HNF1B(C) and MSMB2 comprised the predominant isoforms in benign tissues (90% and 98% of total HNF1B or MSMB expression), HNF1B(B) and MSMB1 were predominant in malignant tissue (95% and 96% of total HNF1B or MSMB expression; P = 1.7 x 10(-7) and 4 x 10(-4) respectively), indicating major shifts in isoform usage.

conclusionsOur results indicate that the amount or nature of mRNA transcripts expressed from the LMTK2, HNF1B and MSMB candidate genes is altered in prostate cancer, and provides further evidence for a role for these genes in this disorder. The alterations in isoform usage we detect highlights the potential importance of alternative mRNA processing and moderation of mRNA stability as potentially important disease mechanisms.

Indexed as

AdenocarcinomaAgedAged, 80 and overGenetic Predisposition to DiseaseGenotypeHepatocyte Nuclear Factor 1-betaHumansMaleMembrane ProteinsPolymorphism, Single NucleotideProstateProstatic HyperplasiaProstatic NeoplasmsProstatic Secretory ProteinsProtein IsoformsProtein Serine-Threonine Kinasesbeta-microseminoproteinHepatocyte Nuclear Factor 1-betaHNF1B protein, humanLMTK2 protein, humanMembrane ProteinsProstatic Secretory ProteinsProtein IsoformsProtein Serine-Threonine KinasesRNA, Messenger

Identifiers

PMID20569440
PMCPMC2908099
OpenAlexW2050182534

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.