Evidence map›Paper›PMID 23696788›Full record

ArticlePloS one2013

Tumor derived mutations of protein tyrosine phosphatase receptor type k affect its function and alter sensitivity to chemotherapeutics in glioma.

Supreet Agarwal, Maha S Al-Keilani, Mohammad A Y Alqudah, Zita A Sibenaller, Timothy C Ryken, Mahfoud Assem

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  11. Protein Tyrosine Phosphatases as Potential Regulators of STAT3 Signaling.International journal of molecular sciences · 2018
    Review
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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

6 authors at 2 institutions in 1 country.

Supreet AgarwalPharmaceutics and Translational Therapeutics, College of Pharmacy, University of Iowa, Iowa City, Iowa, United States of America.
Maha S Al-Keilani
Mohammad A Y Alqudah
Zita A Sibenaller
Timothy C Ryken
Mahfoud Assem
University of Iowa · USTranslational Therapeutics (United States) · US

Funding

UNIVERSITY OF IOWA CTSA FOR PEDIATRIC RESEARCHUL1RR024979 · NCRR · UNIVERSITY OF IOWA · PI ROSENTHAL, GARY E · 2007 to 2011
$31.8M
NCRR NIH HHS UL1 RR024979NCRR NIH HHS UL1RR024979
6 · The paper itself

Abstract

Poor prognosis and resistance to therapy in malignant gliomas is mainly due to the highly dispersive nature of glioma cells. This dispersive characteristic results from genetic alterations in key regulators of cell migration and diffusion. A better understanding of these regulatory signals holds promise to improve overall survival and response to therapy. Using mapping arrays to screen for genomic alterations in gliomas, we recently identified alterations of the protein tyrosine phosphatase receptor type kappa gene (PTPRK) that correlate to patient outcomes. These PTPRK alterations are very relevant to glioma biology as PTPRK can directly sense cell-cell contact and is a dephosphorylation regulator of tyrosine phosphorylation signaling, which is a major driving force behind tumor development and progression. Subsequent sequencing of the full length PTPRK transcripts revealed novel PTPRK gene deletion and missense mutations in numerous glioma biopsies. PTPRK mutations were cloned and expressed in PTPRK-null malignant glioma cells. The effect of these mutations on PTPRK anti-oncogenic function and their association with response to anti-glioma therapeutics, such as temozolomide and tyrosine kinase inhibitors, was subsequently analyzed using in vitro cell-based assays. These genetic variations altered PTPRK activity and its post-translational processing. Reconstitution of wild-type PTPRK in malignant glioma cell lines suppressed cell growth and migration by inhibiting EGFR and β-catenin signaling and improved the effect of conventional therapies for glioma. However, PTPRK mutations abrogated tumor suppressive effects of wild-type PTPRK and altered sensitivity of glioma cells to chemotherapy.

Indexed as

Antineoplastic AgentsCell Line, TumorCell MovementCell ProliferationDacarbazineEnzyme InhibitorsGliomaHumansMutationReceptor-Like Protein Tyrosine Phosphatases, Class 2Signal TransductionTemozolomideAntineoplastic AgentsDacarbazineEnzyme InhibitorsReceptor-Like Protein Tyrosine Phosphatases, Class 2Temozolomide

Identifiers

PMID23696788
PMCPMC3656086
OpenAlexW2014716867

What OpenQuestion holds

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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.