Evidence map›Paper›PMID 20015382›Full record

ArticleMolecular cancer2009

The protein tyrosine phosphatase receptor type R gene is an early and frequent target of silencing in human colorectal tumorigenesis.

Mirco Menigatti, Elisa Cattaneo, Jacob Sabates-Bellver, Valery V Ilinsky, Philip Went, Federico Buffoli, Victor E Marquez, Josef Jiricny, Giancarlo Marra

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. [Risk modeling based on HER-2 related genes for bladder cancer survival prognosis assessment].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  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

9 authors at 5 institutions in 4 countries.

Mirco MenigattiInstitute of Molecular Cancer Research, University of Zurich, Switzerland. menigatti@imcr.uzh.ch
Elisa Cattaneo
Jacob Sabates-Bellver
Valery V Ilinsky
Philip Went
Federico Buffoli
Victor E Marquez
Josef Jiricny
Giancarlo Marra
University of Zurich · CHFondazione Poliambulanza Istituto Ospedaliero · ITInstitute of Cancer Research · GBNational Cancer Institute · USTriemli Hospital · CH

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

backgroundTumor development in the human colon is commonly accompanied by epigenetic changes, such as DNA methylation and chromatin modifications. These alterations result in significant, inheritable changes in gene expression that contribute to the selection of tumor cells with enhanced survival potential.

resultsA recent high-throughput gene expression analysis conducted by our group identified numerous genes whose transcription was markedly diminished in colorectal tumors. One of these, the protein-tyrosine phosphatase receptor type R (PTPRR) gene, was dramatically downregulated from the earliest stages of cellular transformation. Here, we show that levels of both major PTPRR transcript variants are markedly decreased (compared with normal mucosal levels) in precancerous and cancerous colorectal tumors, as well in colorectal cancer cell lines. The expression of the PTPRR-1 isoform was inactivated in colorectal cancer cells as a result of de novo CpG island methylation and enrichment of transcription-repressive histone-tail marks, mainly H3K27me3. De novo methylation of the PTPRR-1 transcription start site was demonstrated in 29/36 (80%) colorectal adenomas, 42/44 (95%) colorectal adenocarcinomas, and 8/8 (100%) liver metastases associated with the latter tumors.

conclusionsEpigenetic downregulation of PTPRR seems to be an early alteration in colorectal cell transformation, which is maintained during the clonal selection associated with tumor progression. It may represent a preliminary step in the constitutive activation of the RAS/RAF/MAPK/ERK signalling, an effect that will later be consolidated by mutations in genes encoding key components of this pathway.

Indexed as

Gene SilencingAdenocarcinomaColorectal NeoplasmsDNA MethylationHumansReceptor-Like Protein Tyrosine Phosphatases, Class 7RNA, MessengerPTPRR protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 7RNA, Messenger

Identifiers

PMID20015382
PMCPMC2801661
OpenAlexW2124618732

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.