ReviewOncology reviews2012
Mechanisms of virus immune evasion lead to development from chronic inflammation to cancer formation associated with human papillomavirus infection.
Review in Oncology reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed.
- Increasing intrinsic protein disorder improves CD8+ immunogenicity for a SARS CoV2 vaccine candidate antigen.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Within host dynamics of HPV infection with cellular immunity and HPV-infected dormant cells reactivation.Infectious Disease Modelling · 2026Article
- Basic Clinical Bidirectional Empowerment: Synergistic Breakthrough in Molecular Mechanisms and Clinical Management of Small Cell Cervical Carcinoma.International journal of molecular sciences · 2026Review
- Estrogen receptor α (mBio · 2026Article
- Role of soluble human leukocyte antigen-G in virus-associated cancers: A focused minireview.World journal of virology · 2026Review
- TRIM71 suppresses cervical cancer progression by inhibiting Nectin4-mediated Wnt/β-catenin signaling.Biology direct · 2026Article
- The Microbiome-Mitochondria-Extracellular Vesicle Axis in HPV Persistence and Cervical Carcinogenesis.Genes · 2026Review
- Recent advances in human papillomavirus vaccines and therapeutic strategies: Combating cervical and non-cervical cancers.Genes & diseases · 2026Review
- An Overview of the Mechanisms of HPV-Induced Cervical Cancer: The Role of Kinase Targets in Pathogenesis and Drug Resistance.Cancers · 2026Review
- Attributes of HPV associated cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- HPV-Independent Cervical Cancer-A New Challenge of Modern Oncology.International journal of molecular sciences · 2025Review
- Harnessing the Power of Microbiota: How Do KeyBiology · 2025Review
- Review
- Article
- Unraveling HPV-associated cancer complexity: From molecular insights to innovative therapies.Heliyon · 2025Review
- Regulation of Granzymes A and B by High-Risk HPV: Impact on Immune Evasion and Carcinogenesis.Viruses · 2025Review
- The Relationship Between Cervicovaginal Infection, Human Papillomavirus Infection and Cervical Intraepithelial Neoplasia in Romanian Women.Diseases (Basel, Switzerland) · 2025Article
- Understanding the role of oral and vaginal microbiomes in HPV-related cervical, head, and neck cancers: knowledge gaps and feasibility in Sub-Saharan Africa.Frontiers in microbiomes · 2025Review
- Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment.Frontiers in immunology · 2025Review
- Integrative Analysis of Shared Pathogenic Genes and Potential Mechanisms inMediators of inflammation · 2025Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human papillomavirus (HPV) has developed strategies to escape eradication by innate and adaptive immunity. Immune response evasion has been considered an important aspect of HPV persistence, which is the main contributing factor leading to HPV-related cancers. HPV-induced cancers expressing viral oncogenes E6 and E7 are potentially recognized by the immune system. The major histocompatibility complex (MHC) class I molecules are patrolled by natural killer cells and CD8+ cytotoxic T lymphocytes, respectively. This system of recognition is a main target for the strategies of immune evasion deployed by viruses. The viral immune evasion proteins constitute useful tools to block defined stages of the MHC class I presentation pathway, and in this way HPV avoids the host immune response. The long latency period from initial infection to persistence signifies that HPV evolves mechanisms to escape the immune response. It has now been established that there are oncogenic mechanisms by which E7 binds to and degrades tumor suppressor Rb, while E6 binds to and inactivates tumor suppressor p53. Therefore, interaction of p53 and pRb proteins can give rise to an increased immortalization and genomic instability. Overexpression of NF-κB in cervical and penile cancers suggests that NF-κB activation is a key modulator in driving chronic inflammation to cancer. HPV oncogene-mediated suppression of NF-κB activity contributes to HPV escape from the immune system. This review focuses on the diverse mechanisms of the virus immune evasion with HPV that leads to chronic inflammation and cancer.
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.