ArticleInternational journal of cancer2018
Molecular progression to cervical precancer, epigenetic switch or sequential model?
Article in International journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Methylation of Host and/or Human Papillomavirus (HPV) DNA in Management of Cervical Intraepithelial Neoplasia Grade 2 (CIN2) Lesions.International journal of molecular sciences · 2023Pooled it
- Combined HPV 16 E2 and L1 methylation predict response to treatment with cidofovir and imiquimod in patients with vulval intraepithelial neoplasia.Cancer biomarkers : section A of Disease markers · 2022Trial
- DNA methylation for cervical cancer screening: a training set in China.Clinical epigenetics · 2020Trial
- A Holistic Framework for Cervical Cancer Screening and Risk Stratification: Integrating Etiology, Morphology, Epigenetics, and Microecology.Cancer management and research · 2026Review
- A longitudinal pilot study in pre-menopausal women links cervicovaginal microbiome to CIN3 progression and recovery.Communications biology · 2025Article
- Recent advances on gene-related DNA methylation in cancer diagnosis, prognosis, and treatment: a clinical perspective.Clinical epigenetics · 2025Review
- Molecular Insights Into the Natural History of Anal HSIL.Journal of medical virology · 2025Article
- Advances in human papillomavirus detection for cervical cancer screening and diagnosis: challenges of conventional methods and opportunities for emergent tools.Analytical methods : advancing methods and applications · 2025Review
- Limited confidence in cervical cancer screening - unusually increased carcinoembryonic antigen expression resulting in the rapid development of cervical intraepithelial neoplasia grade 2.Archives of medical science : AMS · 2025Article
- The current state of DNA methylation biomarkers in self-collected liquid biopsies for the early detection of cervical cancer: a literature review.Infectious agents and cancer · 2024Article
- Article
- HPV induced R-loop formation represses innate immune gene expression while activating DNA damage repair pathways.PLoS pathogens · 2024Article
- High frequency of alpha7-HPV in Colombian Caribbean coast women: cervical cancer screening analysis.BMC infectious diseases · 2024Article
- DNA methylation as a triage tool for cervical cancer screening - A meeting report.Preventive medicine reports · 2024Review
- Detection of cervical precancerous lesions and cancer by small-scale RT-qPCR analysis of oppositely deregulated mRNAs pairs in cytological smears.Frontiers in oncology · 2024Article
- The Role of p16/Ki67 Dual Staining in Cervical Cancer Screening.Current issues in molecular biology · 2023Review
- Assessing the risk of cervical neoplasia in the post-HPV vaccination era.International journal of cancer · 2023Review
- DNA methylation testing with S5 for triage of high-risk HPV positive women.International journal of cancer · 2022Article
- Clinical performance of methylation as a biomarker for cervical carcinoma in situ and cancer diagnosis: A worldwide study.International journal of cancer · 2022Article
- Consistency of the S5 DNA methylation classifier in formalin-fixed biopsies versus corresponding exfoliated cells for the detection of pre-cancerous cervical lesions.Cancer medicine · 2021Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The evolution of precancerous cervical lesions is poorly understood. A widely held model of cervical intraepithelial neoplasia grade 3 (CIN3) development is sequential progression from normal through CIN1 and CIN2 to CIN3. Another hypothesis, the "molecular switch" model, postulates that CIN3 can evolve directly from human papillomavirus (HPV)-infected normal epithelium without progressing through CIN1 and CIN2. To shed light on this process, we compared DNA methylation of selected human biomarkers and HPV types in two groups of CIN1: CIN1 that were near or adjacent to CIN3 (adjacent-CIN1) and CIN1 that were the principal lesions with no CIN3 detected (principal-CIN1). 354 CIN (CIN1 and CIN3) and normal tissue areas were dissected and typed for HPV from 127 women who underwent loop electrosurgical excision procedures (LEEP). Methylation of genes EPB41L3 and the viral regions of HPV16-L1/L2, HPV18-L2, HPV31-L1, and HPV33-L2 were determined by a highly accurate quantitative pyrosequencing of bisulfite converted DNA. There was a significant trend of increased methylation with disease grade comparing normal to CIN1 and CIN3 (p < 0.0001). Adjacent-CIN1 predominantly shared the same HPV types as the CIN3, however, methylation differed substantially between adjacent-CIN1 and CIN3 (p = 0.008). In contrast diagnostically principal-CIN1 had an indistinguishable methylation distribution compared to adjacent-CIN1 (EPB41L3: p = 0.49; HPVme-All: p = 0.11). Our results suggest that progression from normal epithelium to CIN1 or CIN3 is usually promoted by the same HPV type but occurs via distinct DNA epigenotypes, thus favoring the "molecular switch" model.
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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.