ArticleThe open virology journal2012
Loss of HPV16 E2 Protein Expression Without Disruption of the E2 ORF Correlates with Carcinogenic Progression.
Article in The open virology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 34 citations in OpenAlex.
- HPV Integration in Head and Neck Cancer: Downstream Splicing Events and Expression Ratios Linked with Poor Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Human papilloma virus integration sites and genomic signatures in head and neck squamous cell carcinoma.Molecular oncology · 2022Article
- Targeted RNA next generation sequencing analysis of cervical smears can predict the presence of hrHPV-induced cervical lesions.BMC medicine · 2022Article
- Proton-induced DNA damage promotes integration of foreign plasmid DNA into human genome.Frontiers in oncology · 2022Article
- Article
- The CXCL12/CXCR4 Signaling Pathway: A New Susceptibility Factor in Human Papillomavirus Pathogenesis.PLoS pathogens · 2016Article
- HPV16-E2 induces prophase arrest and activates the cellular DNA damage response in vitro and in precursor lesions of cervical carcinoma.Oncotarget · 2015Article
- Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells.Virus genes · 2015Article
- Genome-wide analysis of high risk human papillomavirus E2 proteins in human primary keratinocytes.Genomics data · 2014Article
- HPV16 E2-mediated potentiation of NF-κB activation induced by TNF-α involves parallel activation of STAT3 with a reduction in E2-induced apoptosis.Molecular and cellular biochemistry · 2014Article
- Therapeutic Vaccine Strategies against Human Papillomavirus.Vaccines · 2014Review
- New HPV16 viral biomarkers to understand the progression of cervical lesions towards cancer.The Indian journal of medical research · 2014Article
- Physical state & copy number of high risk human papillomavirus type 16 DNA in progression of cervical cancer.The Indian journal of medical research · 2014Article
- Viral load, integration and methylation of E2BS3 and 4 in human papilloma virus (HPV) 16-positive vaginal and vulvar carcinomas.PloS one · 2014Article
- Sequence variation in the E2-binding domain of HPV16 and biological function evaluation in Tunisian cervical cancers.BioMed research international · 2014Article
- E2 proteins of high risk human papillomaviruses down-modulate STING and IFN-κ transcription in keratinocytes.PloS one · 2014Article
- ONCOGENIC HUMAN PAPILLOMAVIRUSES: High-Risk Human Papillomaviruses: Towards a Better Understanding of the Mechanisms of Viral Transformation, Latency and Immune-Escape.The open virology journal · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integration of the viral DNA in the cellular genome has been suggested to be critical in carcinogenic progression of HPV-associated cervical neoplasia. This event can be accompanied by disruption of the open reading frame (ORF) encoding the E2 repressor, thus leading to transcriptional up-regulation of the E6 and E7 viral oncogenes. At this stage, it is unclear whether disruption of the E2 ORF is mandatory for carcinogenic progression. We measured E2 RNA and protein expression in clinical samples of various grades of HPV16-associated cervical neoplasia and compared it with the status of the viral genome. RNA extracted from paraffin embedded tissues was hybridized to specific probes and quantified by the NanoString technology. Protein expression was appreciated by immunohistochemistry and the status of viral DNA was determined by in situ hybridization, all performed on serial sections of the same samples. E2 protein was found highly expressed in CIN1, CIN2 lesions where the HPV DNA was highly replicative, while it was decreased in more advanced grade lesions where replication is decreased or lost (CIN3 and SCC). In contrast, E2 transcripts could be elevated even in conditions of no or low expression of the protein, as found in the Caski cell line. Our data demonstrate that integration of the viral DNA in the cellular genome does not always lead to disruption of the E2 ORF and drastic reduction of E2 transcripts, while in contrast, expression of the E2 protein is always drastically reduced.
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.