Evidence map›Paper›PMID 25138050›Full record

ArticleOncotarget2014

Deletion of Ptprd and Cdkn2a cooperate to accelerate tumorigenesis.

Berenice Ortiz, Julie R White, Wei H Wu, Timothy A Chan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 23% 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, 23 citations in OpenAlex.

  1. Trial
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  4. Decreased HLF Expression Predicts Poor Survival in Lung Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
  5. Association ofFrontiers in oncology · 2021
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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.

Berenice OrtizGerstner Sloan-Kettering Graduate School, Memorial Sloan-Kettering Cancer Center, New York, NY, USA; Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Julie R WhiteThe Tri-Institutional Laboratory of Comparative Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Wei H WuHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Timothy A ChanHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA; Dept. of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA; Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
Memorial Sloan Kettering Cancer Center · USTri-Institutional PhD Program in Chemical Biology · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Elucidating the function of the widely inactivated phosphatase PTPRD in the molecR01CA154767 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI CHAN, TIMOTHY AN-THY · 2011 to 2015
$1.9M
Molecular mediators of tumor suppression for the PTPRD phosphatase in gliomasF31CA171566 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI ORTIZ, BERENICE · 2012 to 2013
$82k
NCI NIH HHS F31 CA171566NCI NIH HHS F31CA171566NCI NIH HHS P30 CA008748NCI NIH HHS P30CA008748NCI NIH HHS R01 CA154767NCI NIH HHS R01CA154767
6 · The paper itself

Abstract

PTPRD encodes the protein tyrosine phosphatase receptor type D and is frequently inactivated across many human cancers. Despite its frequent inactivation, it is unknown whether loss of PTPRD promotes tumorigenesis in vivo. PTPRD is located on chromosome 9p, as is CDKN2A, and the two loci are frequently deleted together. Here, we show that co-deletion of Ptprd and Cdkn2a cooperate to accelerate tumorigenesis. Interestingly,heterozygous loss of Ptprd was sufficient to promote tumorigenesis in our model, suggesting that Ptprd may be a haploinsufficient tumor suppressor. The loss of Ptprd resulted in changes to the tumor spectrum in mice and increased the frequency of lymphomas. In total, we reveal that Ptprd is a tumor suppressor that can promote tumorigenesis in concert with Cdkn2a loss.

Indexed as

AnimalsCarcinogenesisCyclin-Dependent Kinase Inhibitor p16Gene Expression Regulation, NeoplasticGenes, Tumor SuppressorGenotyping TechniquesHumansLoss of HeterozygosityMiceMice, Inbred C57BLMice, KnockoutReceptor-Like Protein Tyrosine Phosphatases, Class 2SarcomaCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16PTPRD protein, humanPtprd protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 2

Identifiers

PMID25138050
PMCPMC4196177
OpenAlexW1869167622

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.