ArticleVirology2013
Epigenetics of human papillomaviruses.
Article in Virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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.
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.
Who cites it
57 citing papers in PubMed, 116 citations in OpenAlex.
- DNA Methylation in Cervical Intraepithelial Neoplasia and Cervical Cancer: Triage and Management.Current topics in microbiology and immunology · 2026Review
- Evaluating PAX1/JAM3 methylation for triage in HPV 16/18-infected women.Clinical epigenetics · 2024Article
- NS1-mediated DNMT1 degradation regulates human bocavirus 1 replication and RNA processing.PLoS pathogens · 2024Article
- Cis-regulatory effect of HPV integration is constrained by host chromatin architecture in cervical cancers.Molecular oncology · 2024Article
- Identification of a novel papillomavirus in oral swabs from giant pandas (Frontiers in veterinary science · 2024Article
- Nuclear proinflammatory cytokine S100A9 enhances expression of human papillomavirus oncogenes via transcription factor TEAD1.Journal of virology · 2023Article
- Human papillomavirus integration transforms chromatin to drive oncogenesis.Genome biology · 2023Article
- Investigation of molecular mechanisms underlying JAK/STAT signaling pathway in HPV-induced cervical carcinogenesis using 'omics' approach.Medical oncology (Northwood, London, England) · 2022Article
- Searching for the methylation sites involved in human papillomavirus type 16 and 18‑positive women with cervical cancer.Molecular and clinical oncology · 2022Article
- Article
- Detection of Host Cell Gene/HPV DNA Methylation Markers: A Promising Triage Approach for Cervical Cancer.Frontiers in oncology · 2022Review
- Epigenetic and Transcriptomic Regulation Landscape in HPV+ Cancers: Biological and Clinical Implications.Frontiers in genetics · 2022Review
- Comprehensive bioinformatic analysis reveals oncogenic role of H2A.Z isoforms in cervical cancer progression.Iranian journal of basic medical sciences · 2021Article
- Regulation of Human Papillomavirus 18 Genome Replication, Establishment, and Persistence by Sequences in the Viral Upstream Regulatory Region.Journal of virology · 2021Article
- The role of HPV-induced epigenetic changes in cervical carcinogenesis (Review).Biomedical reports · 2021Review
- HPV-Related Promoter Methylation-Based Gene Signature Predicts Clinical Prognosis of Patients With Cervical Cancer.Frontiers in oncology · 2021Article
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- Review
- Tip60 and p300 function antagonistically in the epigenetic regulation of HPV18 E6/E7 genes in cervical cancer HeLa cells.Genes & genomics · 2020Article
- Risk stratification of HPV 16 DNA methylation combined with E6 oncoprotein in cervical cancer screening: a 10-year prospective cohort study.Clinical epigenetics · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human papilllomaviruses (HPVs) are common human pathogens that infect cutaneous or mucosal epithelia in which they cause warts, self-contained benign lesions that commonly regress. The HPV life cycle is intricately tied to the differentiation of the host epithelium it infects. Mucosotropic HPVs are the most common sexually transmitted pathogen known to mankind. A subset of the mucosotropic HPVs, so-called high risk HPVs, is etiologically associated with numerous cancers of the anogenital tract, most notably the cervix, as well as a growing fraction of head and neck cancers. In these cancers, the HPV genome, which normally exists an a double stranded, circular, nuclear plasmid, is commonly found integrated into the host genome and expresses two viral oncogenes, E6 and E7, that are implicated in the development and maintainance of the cancers caused by these high risk HPVs. Numerous studies, primarily on the high risk HPV16, have documented that the methylation status of the viral genome changes not only in the context of the viral life cycle but also in the context of the progressive neoplastic disease that culminates in cancer. In this article, we summarize the knowledge gained from those studies. We also provide the first analysis of available ChIP-seq data on the occupancy of both epigentically modified histones as well as transcription factors on the high risk HPV18 genome in the context of HeLa cells, a cervical cancer-derived cell line that has been the subject of extensive analyses using this technique.
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What OpenQuestion holds
Registered trials
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.