Evidence map›Paper›PMID 30515568›Full record

ArticleJournal of cancer research and clinical oncology2019

PTPN2 deficiency along with activation of nuclear Akt predict endocrine resistance in breast cancer.

Elin Karlsson, Cynthia Veenstra, Jon Gårsjö, Bo Nordenskjöld, Tommy Fornander, Olle Stål

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. PTPN2 in the Immunity and Tumor Immunotherapy: A Concise Review.International journal of molecular sciences · 2022
    Review
  4. Article
  5. Protein Tyrosine Phosphatases: Mechanisms in Cancer.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. 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

6 authors at 2 institutions in 1 country.

Elin KarlssonDepartment of Clinical and Experimental Medicine, Department of Oncology, Linköping University, 58185, Linköping, Sweden.
Cynthia VeenstraDepartment of Clinical and Experimental Medicine, Department of Oncology, Linköping University, 58185, Linköping, Sweden. cynthia.veenstra@liu.se.ORCID http://orcid.org/0000-0002-3084-7881
Jon GårsjöDepartment of Clinical and Experimental Medicine, Department of Oncology, Linköping University, 58185, Linköping, Sweden.
Bo NordenskjöldDepartment of Clinical and Experimental Medicine, Department of Oncology, Linköping University, 58185, Linköping, Sweden.
Tommy FornanderDepartment of Oncology, Karolinska University Hospital and Karolinska Institute, 17176, Stockholm, Sweden.
Olle StålDepartment of Clinical and Experimental Medicine, Department of Oncology, Linköping University, 58185, Linköping, Sweden.
Linköping University · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe protein tyrosine phosphatase, non-receptor type 2 (PTNP2) regulates receptor tyrosine kinase signalling, preventing downstream activation of intracellular pathways like the PI3K/Akt pathway. The gene encoding the protein is located on chromosome 18p11; the 18p region is commonly deleted in breast cancer. In this study, we aimed to evaluate PTPN2 protein expression in a large breast cancer cohort, its possible associations to PTPN2 gene copy loss, Akt activation, and the potential use as a clinical marker in breast cancer.

methodsPTPN2 protein expression was analysed by immunohistochemistry in 664 node-negative breast tumours from patients enrolled in a randomised tamoxifen trial. DNA was available for 146 patients, PTPN2 gene copy number was determined by real-time PCR.

resultsPTPN2 gene loss was detected in 17.8% of the tumours. Low PTPN2 protein expression was associated with higher levels of nuclear-activated Akt (pAkt-n). Low PTPN2 as well as the combination variable low PTPN2/high pAkt-n could be used as predictive markers of poor tamoxifen response.

conclusionPTPN2 negatively regulates Akt signalling and loss of PTPN2 protein along with increased pAkt-n is a new potential clinical marker of endocrine treatment efficacy, which may allow for further tailored patient therapies.

Indexed as

Antineoplastic Agents, HormonalBiomarkers, TumorBreast NeoplasmsDrug Resistance, NeoplasmFemaleGene DosageHumansProtein Tyrosine Phosphatase, Non-Receptor Type 2Proto-Oncogene Proteins c-aktRandomized Controlled Trials as TopicRetrospective StudiesTamoxifenAntineoplastic Agents, HormonalBiomarkers, TumorProtein Tyrosine Phosphatase, Non-Receptor Type 2Proto-Oncogene Proteins c-aktPTPN2 protein, humanTamoxifen18p deletionBreast cancerGene copy numberImmunohistochemistryProtein tyrosine phosphatasePTPN2TCPTP

Identifiers

PMID30515568
PMCPMC6394658
OpenAlexW2902034058

What OpenQuestion holds

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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.