ReviewMolecular diagnosis & therapy2022
Hyperactivating p53 in Human Papillomavirus-Driven Cancers: A Potential Therapeutic Intervention.
Review in Molecular diagnosis & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Rethinking residual p53 function in HPV-positive cervical cancer cells.Journal of virology · 2026Article
- Histone modifications in cervical cancer: Epigenetic mechanisms, functions and clinical implications (Review).Oncology reports · 2025Review
- Deciphering the Expression, Functional Role, and Prognostic Significance ofJournal of obstetrics and gynaecology of India · 2025Article
- Developments and future prospects of personalized medicine in head and neck squamous cell carcinoma diagnoses and treatments.Cancer reports (Hoboken, N.J.) · 2024Review
- Review
- Assessing the Genomic Landscape of Cervical Cancers: Clinical Opportunities and Therapeutic Targets.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Hyperactivation of p53 using CRISPRa kills human papillomavirus-driven cervical cancer cells.Virus genes · 2023Article
- Identification of p53-target genes in human papillomavirus-associated head and neck cancer by integrative bioinformatics analysis.Frontiers in oncology · 2023Article
- Article
- Review
- Editorial: Advances in wild type and mutant p53 research in cancer.Frontiers in molecular biosciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite a vaccine being available, human papillomavirus virus (HPV)-driven cancers remain the ninth most prevalent cancers globally. Current therapies have significant drawbacks and often still lead to poor prognosis and underwhelming survival rates. With gene therapy becoming more available in the clinic, it poses a new front for therapeutic development. A characteristic of HPV-driven cancers is the ability to encode oncoproteins that aberrate normal p53 function without mutating this tumour-suppressor gene. The HPV E6 oncoprotein degrades p53 to allow the HPV-driven carcinogenic process to proceed. This review aimed to investigate the use of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) gene-editing technology and how it may be used to overcome HPV-mediated silencing of p53 by hyper-expressing the p53 promoter. Increasing p53 bioavailability may have promising potential as a therapy and has been a goal in the context of HPV-driven cancers. Clinical trials and proof-of-concept pre-clinical work have shown positive outcomes and tumour death when p53 levels are increased. Despite previous successes of RNA-based medicines, including the knockout of HPV oncogenes, the use of CRISPR activation is yet to be investigated as a promising potential therapy. This short review summarises key developments on attempts that have been made to increase p53 expression in the context of HPV cancer therapy, but leaves open the possibility for other cancers bearing a p53 wild-type gene.
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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.