Evidence map›Paper›PMID 28202002›Full record

ArticleBMC cancer2017

Viral E6 is overexpressed via high viral load in invasive cervical cancer with episomal HPV16.

Die Hong, Jia Liu, Ying Hu, Xiaonan Lu, Baohua Li, Yang Li, Dongxiao Hu, Weiguo Lu, Xing Xie, Xiaodong Cheng

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
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  12. Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  13. Article
  14. Human PapillomavirusPathogens (Basel, Switzerland) · 2020
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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 1 institution in 1 country.

Die HongDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Jia LiuDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Ying HuDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Xiaonan LuDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Baohua LiDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Yang LiDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Dongxiao HuDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Weiguo LuDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Xing XieDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China.
Xiaodong ChengDepartment of Gynecologic Oncology, Women's Hospital, School of Medicine, Women's Reproductive Health Laboratory of Zhejiang Province, Zhejiang University, Xueshi Rd 1#, Hangzhou, 310006, China. chengxd@zju.edu.cn.
Women's Hospital, School of Medicine, Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe integration of HR-HPV genome into host DNA is regarded as a key step for the development of cervical cancer. However, HR-HPV genome indeed exists as episome except for integrant. It may be alternative mechanisms in episome-associated carcinogenesis, although, by which HPV 16 episome induces cervical carcinogenesis is unclear now.

methodsNinety-three invasive cervical cancer tissues with HPV16 positive were collected. Viral physical status was calculated from comparing E2 to E6-copies and detection of viral load was made with realtime-PCR using copy numbers of E6. HPV16 E6 mRNA transcript levels were measured by realtime-PCR. The methylation frequency of HPV16 promoter was detected by PCR and pyrosequencing.

resultsIn 93 samples, 21.5% (20/93) presented purely integrated viral genome, 53.8% (50/93) mixed viral genome, and 24.7% (23/93) purely episomal viral genome. Mean E6 expression in samples with purely episomal viral genomes was 7.13-fold higher than that with purely integrated viral genomes. Meanwhile, viral load in samples with purely episomal viral genomes was 4.53-fold higher than that with purely integrated viral genomes. E6 mRNA expression increased with the viral load in purely episomal cases. There were no differences of mean methylation frequency between purely episomal and integrated virus and among five CpG positions of HPV16 promoter for all samples. And there also was no correlation between E6 mRNA expression and methylation of HPV16 promoter among all samples with purely HPV16 episomal virus.

conclusionsHPV16 with the purely episomal viral genomes exists in a definite proportion of invasive cervical cancer, and episomal HPV16 also overexpresses E6 mRNA, probably through a high level of viral load.

Indexed as

AdultAgedDNA MethylationFemaleGenome, ViralHuman papillomavirus 16HumansMiddle AgedNeoplasm InvasivenessOncogene Proteins, ViralPapillomavirus InfectionsPlasmidsPolymerase Chain ReactionRepressor ProteinsUterine Cervical DysplasiaUterine Cervical NeoplasmsE6 protein, Human papillomavirus type 16Oncogene Proteins, ViralRepressor ProteinsCervical cancerEpisomeHPV16IntegrationOncogene expressionViral load

Identifiers

PMID28202002
PMCPMC5311840
OpenAlexW2588914628

What OpenQuestion holds

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LicenceCC BY
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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.