HPV16Human Papillomavirus Type 16
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References in periodicals archive ?
(2,4,8,9) Documentation of hrHPV status, especially HPV16, in patients with oropharyngeal SCC is becoming critical for clinical management and selection for clinical trials.
HPV16 and HPV18 are the leading viral genotypes that increase cancer risk.
HPV16 oncoproteins induce MMPs/ RECK-TIMP-2 imbalance in primary keratinocytes: possible implications in cervical carcinogenesis.
The distribution was: HPV16 was 4/100 (9%) from OSCC group while HPV 18 was 5/100(11%).
Wu (John Hopkins, Baltimore), this cell line is a murine carcinoma derived from lung epithelium, transduced with HPV16 E6/E7 and c-Ha-ras oncogenes [21].
The STK31 gene targets at oncogene E7 of HPV16. Its promoter/exon 1 is hypomethylated in HPV16/18-positive cervical cell lines, which induces an integration of HPV16E7/ E6 [20].
HPVneg 70% HPV16 15% HPV56 10% HPV18 5% Note: Table made from bar graph.
Studies have shown strong associations with immunosuppression, current or previous tobacco use, toxin/radiation exposure, and trauma.[sup][1] A number of studies have confirmed a causative role for HPV, mostly HPV16, in the development of this tumor.
Fifteen out of these serotypes play an oncogenic role.1 More than 90 percent of head and neck cancer (HNC) is caused by HPV16.2 Depending upon the seriousness, there are three groups of serotypes; low, intermediate and high risk.
Epigenetic changes in HPV16 were also found to occur through the interaction of HPV oncogenes with HAT [59,74].
Among the HPV genotype of high risk, HPV16 is the most prevalent.