Evidence map›Paper›PMID 31595832›Full record

ArticleEpigenetics

PTPRT epigenetic silencing defines lung cancer with STAT3 activation and can direct STAT3 targeted therapies.

Malabika Sen, Audrey Kindsfather, Ludmila Danilova, Feng Zhang, Raffaele Colombo, Matthew G LaPorte, Brenda F Kurland, Donna M Huryn, Peter Wipf, James G Herman

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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  11. Frontiers in molecular biosciences · 2022
    Article
  12. Article
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  14. Frontiers in pharmacology · 2021
    Article
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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

10 authors at 3 institutions in 2 countries.

Malabika SenDepartment of Hematology/Oncology, UPMC Hillman Cancer Center , Pittsburgh, PA, USA.
Audrey KindsfatherDepartment of Hematology/Oncology, UPMC Hillman Cancer Center , Pittsburgh, PA, USA.
Ludmila DanilovaDepartment of Oncology, Laboratory of Systems Biology and Computational Genetics, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine , Baltimore, MD, USA.ORCID 0000-0003-2813-3094
Feng ZhangChemical Diversity Center, University of Pittsburgh , Pittsburgh, PA, USA.
Raffaele ColomboChemical Diversity Center, University of Pittsburgh , Pittsburgh, PA, USA.
Matthew G LaPorteChemical Diversity Center, University of Pittsburgh , Pittsburgh, PA, USA.
Brenda F KurlandDepartment of Biostatistics, University of Pittsburgh , Pittsburgh, PA, USA.ORCID 0000-0002-5669-0595
Donna M HurynChemical Diversity Center, University of Pittsburgh , Pittsburgh, PA, USA.ORCID 0000-0001-5542-4968
Peter WipfChemical Diversity Center, University of Pittsburgh , Pittsburgh, PA, USA.
James G HermanDepartment of Hematology/Oncology, UPMC Hillman Cancer Center , Pittsburgh, PA, USA.
University of Pittsburgh · USUPMC Hillman Cancer Center · USJohns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
NCI NIH HHS P30 CA006973NCI NIH HHS P30 CA047904
6 · The paper itself

Abstract

Signal Transducers and Activators of Transcription-3 (STAT3), a potent oncogenic transcription factor, is constitutively activated in lung cancer, but mutations in pathway genes are infrequent. Protein Tyrosine Phosphatase Receptor-T (PTPRT) is an endogenous inhibitor of STAT3 and PTPRT loss-of-function represents one potential mechanism of STAT3 hyperactivation as observed in other malignancies. We determined the role of PTPRT promoter methylation and sensitivity to STAT3 pathway inhibitors in non-small cell lung cancer (NSCLC). TCGA and Pittsburgh lung cancer cohort methylation data revealed hypermethylation of PTPRT associated with diminished mRNA expression in a subset of NSCLC patients. We report frequent hypermethylation of the PTPRT promoter which correlates with transcriptional silencing of PTPRT and increased STAT3 phosphorylation (Y705) as determined by methylation-specific PCR (MSP) and real time quantitative reverse transcription (RT)-PCR in NSCLC cell lines. Silencing of PTPRT using siRNA in H520 lung cancer cell line resulted in increased pSTAT3

Indexed as

DNA MethylationGene SilencingA549 Cellsbcl-X ProteinCarcinoma, Non-Small-Cell LungCyclin D1HumansLung NeoplasmsPromoter Regions, GeneticReceptor-Like Protein Tyrosine Phosphatases, Class 2STAT3 Transcription FactorBCL2L1 protein, humanbcl-X ProteinCyclin D1PTPRT protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 2STAT3 protein, humanSTAT3 Transcription Factornon-small cell lung cancerPTPRT methylationSTAT3

Identifiers

PMID31595832
PMCPMC7574378
OpenAlexW2979948515

What OpenQuestion holds

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Registered trials

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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.