Evidence map›Paper›PMID 23690972›Full record

ArticlePloS one2013

Analysis of PTEN methylation patterns in soft tissue sarcomas by MassARRAY spectrometry.

Liang Yin, Wei-Juan Cai, Chun-Xia Liu, Yun-Zhao Chen, Jian-Ming Hu, Jin-Fang Jiang, Hong-An Li, Xiao-Bin Cui, Xiang-Yun Chang, Wen Jie Zhang and 2 more

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  5. Review
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  7. Review
  8. Epigenetic regulation of RTK signaling.Journal of molecular medicine (Berlin, Germany) · 2017
    Review
  9. Association of the hypermethylation status of PTEN tumor suppressor gene with the risk of breast cancer among Kurdish population from Western Iran.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. Malignant tumors of the uterine corpus: molecular background of their origin.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. A novel PTEN gene promoter mutation and untypical Cowden syndrome.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013
    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

12 authors at 1 institution in 1 country.

Liang YinDepartment of Pathology and Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, Shihezi, Xinjiang, PR China.
Wei-Juan Cai
Chun-Xia Liu
Yun-Zhao Chen
Jian-Ming Hu
Jin-Fang Jiang
Hong-An Li
Xiao-Bin Cui
Xiang-Yun Chang
Wen Jie Zhang
Kan Sun
Feng Li
Shihezi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Soft tissue sarcomas (STSs) are a rare and fascinating group of diseases that can be subdivided into specific reciprocal translocations in STSs (SRTSs) and nonspecific reciprocal translocations in STSs (NRTSs). PTEN mutations are rare in STSs, suggesting that PTEN expression may be lost by alternative mechanisms such as methylation. In order to reveal whether aberrant PTEN methylation occurs in STSs, MassARRAY Spectrometry was carried to detect methylation patterns of PTEN in STSs. We evaluated methylation levels in 41 CpG sites from -2,515 to -2,186 bp (amplicon A) and -1,786 to -1,416 bp (amplicon B) relative to the translation initiation site in 110 different cases (46 cases of SRTSs, 40 cases of NRTSs, and 24 cases of normal controls). In addition, immunohistochemistry (IHC) was used to detect the loss of PTEN to determine whether PTEN alterations were responsible for decreased PTEN expression. Our data showed that expression of PTEN was diminished in 49 (57%) STSs, whereas the remaining cases (43%) were classified as high expression. Our previous results found that only 2 of 86 cases (2.3%) had a PTEN mutation suggesting that PTEN may be mainly downregulated in STSs by methylation, but not by mutation of PTEN itself. We observed that amplicon A was hypermethylated in STSs with low PTEN expression, whereas normal controls had low methylation levels (P<0.0001), which was not present in amplicon B (P>0.05), nor were there significant differences in the methylation levels in PTEN between SRTS and NRTS cases. The majority of individual CpG units within two amplicons was demonstrated to be hypermethylated. These findings indicate that PTEN hypermethylation is a common event in STSs suggesting that the inactivation of PTEN may be due to hypermethylation in the promoter of PTEN. The aberrant methylation of the CpG sites within PTEN promoter may serve as a potential candidate biomarker for STSs.

Indexed as

Analysis of VarianceCpG IslandsGene Expression Regulation, NeoplasticHumansImmunohistochemistryMass SpectrometryMethylationPolymerase Chain ReactionPolymorphism, Single-Stranded ConformationalPTEN PhosphohydrolaseSarcomaPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID23690972
PMCPMC3656904
OpenAlexW1998384950

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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.