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HPV is believed to cause cancer by integrating its genome into nuclear DNA. Some of the early genes expressed by HPV, such as E6 and E7, act as oncogenes that promote tumor growth and malignant transformation. [17] HPV genome integration can also cause carcinogenesis by promoting genomic instability associated with alterations in DNA copy ...
For instance, in HPV+OPC the HPV E6 and E7 oncogenes merely render the p53 and pRb pathways dormant, leaving open the possibility of reactivation of these pathways by down-regulating (reducing) expression of the oncogenes. This is in contrast to the mutant form of p53 found in HPV-OPC which is associated with treatment resistance. [11]
According to an article published 16 September 2015 in The Lancet, which reviewed the safety, efficacy, and immunogenicity of VGX-3100 in a double-blind, randomized controlled trial (phase 2b) targeting HPV-16 and HPV-18 E6 and E7 proteins for cervical intraepithelial neoplasia 2/3, it is the first therapeutic vaccine to show efficacy against ...
ThinPrep pap smear with group of normal cervical cells on left and HPV-infected cells showing features typical of koilocytes: enlarged (x2 or x3) nuclei and hyperchromasia. A koilocyte is a squamous epithelial cell that has undergone a number of structural changes, which occur as a result of infection of the cell by human papillomavirus (HPV ...
In HPV-positive disease, these genes are less frequently mutated, and the tumour suppressor gene p53 and pRb (protein retinoblastoma) are commonly inactivated by HPV oncoproteins E6 and E7 respectively. [74] In addition, viral infections such as HPV can cause aberrant DNA methylation during cancer development. HPV-positive head and neck cancers ...
HPV genomes integrate into host genome by disruption of E2 ORF, preventing E2 repression on E6 and E7. Thus, viral genome integration into host DNA genome increases E6 and E7 expression to promote cellular proliferation and the chance of malignancy.
HPV contains a protein, E7, which can bind to Rb in much the same way. [24] Rb can be inactivated by phosphorylation, or by being bound to a viral oncoprotein, or by mutations—mutations which prevent oncoprotein binding are also associated with cancer.
1- TG4050 : This neoantigen individualized therapeutic cancer vaccine is currently being developed in a randomized Phase I/II trial in the adjuvant treatment of head and neck cancer [11]. 2- TG4001 : is a therapeutic vaccine designed to express the E6 and E7 antigens of the HPV-16 virus (human papillomavirus type 16). [12]