ReviewInternational journal of experimental pathology2001
Biology of human papillomaviruses.
Review in International journal of experimental pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 248 citations in OpenAlex.
- Racial and ethnic differences in HPV-related cancer incidence in the United States, 2001-2020.Journal of the National Cancer Institute · 2025Article
- Changes in incidence of HPV-related cancers in South Africa (2011-21): a cross-sectional analysis of the South African National Cancer Registry.The Lancet. Global health · 2025Article
- Role of L1 HPV Protein Expression in the Cytological Diagnosis of Precancerous Cervical Lesions.Journal of clinical medicine · 2025Review
- Mechanisms of Viral DNA Replication of Human Papillomavirus: E2 Protein-Dependent Recruitment of E1 DNA Helicase to the Origin of DNA Replication.International journal of molecular sciences · 2025Article
- De-Escalation Strategies in HPV-Associated Oropharynx Cancer: A Historical Perspective with Future Direction.Cancers · 2024Review
- B7H4 Role in Solid Cancers: A Review of the Literature.Cancers · 2024Review
- CUL4A silencing attenuates cervical carcinogenesis and improves Cisplatin sensitivity.Molecular and cellular biochemistry · 2024Article
- The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus.Biology · 2024Review
- DNA from multiple viral species is associated with Alzheimer's disease risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- The state of human papillomavirus research in Africa.Public health challenges · 2023Review
- Human Papilloma Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Article
- Article
- Effects of Religious Practice and Teachings about Sexual Behavior on Intent to Vaccinate against Human Papillomavirus.Vaccines · 2022Article
- Pathogens and Carcinogenesis: A Review.Biology · 2021Review
- Review
- CRISPR-Cas9: A Preclinical and Clinical Perspective for the Treatment of Human Diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Review
- Global gene methylation profiling of common warts caused by human papillomaviruses infection.Saudi journal of biological sciences · 2021Article
- In Vitro Organotypic Systems to Model Tumor Microenvironment in Human Papillomavirus (HPV)-Related Cancers.Cancers · 2020Review
- Host proteome linked to HPV E7-mediated specific gene hypermethylation in cancer pathways.Infectious agents and cancer · 2020Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human papillomaviruses (HPVs) cause squamous cancers of epithelial surfaces, of which genital cancers are the most common. In this article we have attempted to describe the properties and functions of the viral proteins of HPV type 16, a common cause of genital cancers, and have tried to suggest how their expression may lead to a dysregulated cell which may become malignant. These viruses are attempting to replicate in terminally differentiating keratinocytes and must stimulate G1 to S-phase progression for the replication of their genome. As part of the successful completion of replication and assembly of infectious virus particles, the virus needs at least partial differentiation to occur. Therefore, at the same time as differentiation is occurring, the nuclei of infected cells are in S-phase. While the mechanisms of action of the viral proteins are not completely understood, researchers are making progress and this article strives to bring together the conclusions from some of this work.
Indexed as
Identifiers
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.