Evidence map›Paper›PMID 26057381›Full record

ArticlePloS one2015

Methylated Host Cell Gene Promoters and Human Papillomavirus Type 16 and 18 Predicting Cervical Lesions and Cancer.

Nina Milutin Gašperov, Ivan Sabol, Pavao Planinić, Goran Grubišić, Ivan Fistonić, Ante Ćorušić, Magdalena Grce

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Methylation of Immune Gene Promoters in Oral and Oropharyngeal Cancer.International journal of molecular sciences · 2023
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Limited Role of Promoter Methylation ofChinese medical journal · 2018
    Article
  9. Review
  10. Identification ofFrontiers in genetics · 2018
    Article
  11. Article
  12. Article
  13. Review
  14. 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

7 authors at 2 institutions in 1 country.

Nina Milutin GašperovRudjer Boskovic Institute, Division of Molecular Medicine, Zagreb, Croatia.
Ivan SabolRudjer Boskovic Institute, Division of Molecular Medicine, Zagreb, Croatia.
Pavao PlaninićDepartment of Gynecologic Oncology, Clinic for Gynecology and Obstetrics, Clinical Hospital Center Zagreb, Zagreb, Croatia.
Goran GrubišićObstetrics and Gynaecology Clinic, Clinical Hospital "Sestre milosrdnice," Zagreb, Croatia.
Ivan FistonićPrivate Gynaecological Clinic, Zagreb, Croatia.
Ante ĆorušićDepartment of Gynecologic Oncology, Clinic for Gynecology and Obstetrics, Clinical Hospital Center Zagreb, Zagreb, Croatia.
Magdalena GrceRudjer Boskovic Institute, Division of Molecular Medicine, Zagreb, Croatia.
Rudjer Boskovic Institute · HRUniversity Hospital Centre Zagreb · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Change in the host and/or human papillomavirus (HPV) DNA methylation profile is probably one of the main factors responsible for the malignant progression of cervical lesions to cancer. To investigate those changes we studied 173 cervical samples with different grades of cervical lesion, from normal to cervical cancer. The methylation status of nine cellular gene promoters, CCNA1, CDH1, C13ORF18, DAPK1, HIC1, RARβ2, hTERT1, hTERT2 and TWIST1, was investigated by Methylation Specific Polymerase Chain Reaction (MSP). The methylation of HPV18 L1-gene was also investigated by MSP, while the methylated cytosines within four regions, L1, 5'LCR, enhancer, and promoter of the HPV16 genome covering 19 CpG sites were evaluated by bisulfite sequencing. Statistically significant methylation biomarkers distinguishing between cervical precursor lesions from normal cervix were primarily C13ORF18 and secondly CCNA1, and those distinguishing cervical cancer from normal or cervical precursor lesions were CCNA1, C13ORF18, hTERT1, hTERT2 and TWIST1. In addition, the methylation analysis of individual CpG sites of the HPV16 genome in different sample groups, notably the 7455 and 7694 sites, proved to be more important than the overall methylation frequency. The majority of HPV18 positive samples contained both methylated and unmethylated L1 gene, and samples with L1-gene methylated forms alone had better prognosis when correlated with the host cell gene promoters' methylation profiles. In conclusion, both cellular and viral methylation biomarkers should be used for monitoring cervical lesion progression to prevent invasive cervical cancer.

Indexed as

AdultBiomarkersCell LineCervix UteriCpG IslandsCytosineDNA MethylationDNA, ViralFemaleGene Expression Regulation, ViralHuman papillomavirus 16Human papillomavirus 18HumansMiddle AgedPapillomavirus InfectionsPromoter Regions, GeneticBiomarkersCytosineDNA, Viral

Identifiers

PMID26057381
PMCPMC4461273
OpenAlexW569157409

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.