ArticleOncology letters2015
Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review).
Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
What it found
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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
121 citing papers in PubMed, 185 citations in OpenAlex.
- Engineered T cells targeting E7 mediate regression of human papillomavirus cancers in a murine model.JCI insight · 2018Trial
- Association of serum cytokines with oral HPV clearance.Cytokine · 2016Trial
- Does acute inflammation triggered by infection promote cancer progression?PLoS biology · 2026Review
- Development of a multiplex quantitative real-time PCR (qPCR) assay for simultaneous detection of Schistosoma haematobium and high-risk human papillomaviruses.PLoS neglected tropical diseases · 2026Article
- Polyendocrine Metabolic Ovarian Syndrome (PMOS; Formerly Polycystic Ovary Syndrome/PCOS) and Susceptibility to Microbial Infections: Mechanisms, Clinical Management, and Reproductive Consequences - A Comprehensive Review.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Short-term HPV detection dynamics across hormonal contraceptive methods in adolescent girls and young women: a secondary analysis of a randomized trial in South Africa.Research square · 2026Article
- Synergistic cytotoxicity of recombinant IGFBP-3 and cisplatin in HPV18-positive HeLa cellsResearch in pharmaceutical sciences · 2026Article
- The interplay between HPV, vaginal microbiota and host immunity in cervical carcinogenesis.Discover oncology · 2026Review
- HPV Infection and Oxidative Stress in Cervical Carcinogenesis: Linking Apoptosis, Senescence, SASP, and EMT.Antioxidants (Basel, Switzerland) · 2026Review
- Systemic Immune-Inflammation Markers Associate With Cervical Human Papillomavirus Infection in Asymptomatic Women.Open forum infectious diseases · 2026Article
- Cell-Mediated Immunity Against Human Papillomavirus Infection: From Viral Clearance to Oncogenesis.Viruses · 2026Review
- Metabolism-Driven Modulation by the Human Microbiota: Implications for Cancer Therapy and Emerging Strategies.Advances in experimental medicine and biology · 2026Review
- Deciphering HPV-Associated Immune Evasion in Cervical Cancer Through Multi-Omics Profiling and Computational Screening.Analytical cellular pathology (Amsterdam) · 2026Article
- Hypoxic adaptation theory of cancer.Frontiers in cell and developmental biology · 2026Article
- Expression Analysis of the orphan receptors GPR161, GPR132, GPR20, and GPR139 in patients with cervicitis and low-grade, and high-grade squamous intraepithelial lesions.Genetics and molecular biology · 2026Article
- HPV-driven inflammatory pathways in ovarian carcinogenesis: molecular mechanisms and emerging therapeutic interventions.Journal of ovarian research · 2025Review
- Review
- Epstein-barr virus (EBV) in cervical carcinoma detected by in situ hybridization targeting ebers and the viral genome.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025Article
- From inflammation to invasion: neutrophils in cervical cancer pathogenesis.Annals of medicine and surgery (2012) · 2025Review
- Association between human papillomavirus and behaviour, clinicopathology, and cervical cancer outcome in Zimbabwean women: a cross-sectional study.Reproductive health · 2025Article
61 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
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a defense strategy against invading agents and harmful molecules that is activated immediately following a stimulus, and involves the release of cytokines and chemokines, which activate the innate immune response. These mediators act together to increase blood flow and vascular permeability, facilitating recruitment of effector cells to the site of injury. Following resolution of the injury and removal of the stimulus, inflammation is disabled, but if the stimulus persists, inflammation becomes chronic and is strongly associated with cancer. This is likely to be due to the fact that the inflammation leads to a wound that does not heal, requiring a constant renewal of cells, which increases the risk of neoplastic transformation. Debris from phagocytosis, including the reactive species of oxygen and nitrogen that cause damage to DNA already damaged by the leukotrienes and prostaglandins, has an impact on inflammation and various carcinogenic routes. There is an association between chronic inflammation, persistent infection and cancer, where oncogenic action is mediated by autocrine and paracrine signals, causing changes in somatic cells under the influence of the microbial genome or of epigenetic factors. Among the infectious agents associated with cancer, certain genotypes of human papillomavirus (HPV) stand out. HPV is responsible for virtually all cases of cervical cancer and a lower proportion of cancers of the vagina, vulva, anus, penis and a number of extragenital cancers. In the present review, recent advances in the mechanisms involved in the inflammatory response are presented with their participation in the process of carcinogenesis, emphasizing the role of chronic inflammation in the development of HPV-induced cervical cancer.
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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.