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Introduction. Papillomavirus-induced cancers are addicted to the expression of the major viral oncogenes, E6 and E7, whose combined effect is required for the development and maintenance of the transformed phenotype (reviewed in Ref. [ 1 ]). Abrogation of E6 and E7 expression in tumours, or in cell-lines derived from tumours, results in growth.
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Human Papillomavirus Genome and Its Integration Into the Host Cellular Genome. The HPV genome structure and the oncogenes have been discussed in this section with reference to high-risk HPV16 type (Figure 1).The HPV16 genome is a 7.9 kb long nucleotide belt, segmented into three sections: the early gene-coding region (E), the late gene-coding region (L), and the long control region (LCR), also.
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Cervical carcinogenesis is mediated by the HPV-E6 and E7 oncoproteins, considered as biomarkers usable in managing screen-positive women. We conducted a systematic review and meta-analysis.
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Evasion of Growth Suppressors. Both E6 and E7 contribute to achieve uncontrolled proliferation through deregulation of growth suppressors. E6 targets an important growth suppressor, p53, while pRb is one of the major targets of E7 among few others. It has been diagrammatically illustrated in Figure 2.
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Many discovery approaches to find HPV associated cervical cancer screening biomarkers are currently underway, of which the HR-HPV E6/E7 mRNA test is a promising non-invasive biomarker for the detection of high grade cervical lesion (CIN2+) enabling detection of the HPV infection and simultaneously predicting the change of cervical lesions [32.
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Schematic representation of HPV oncoproteins E5, E6 and E7. HPV16-E5 is an 83-amino acid-long transmembrane protein with three transmembrane domains (TMDI-III). HPV-16 E6 is an 158 amino acid protein with two CXXC (Cys-X-X-Cys,) motifs, which participate in coordinating with zinc ions and are indicated in the schematic.
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Background Genital infection with certain types of Human papillomavirus (HPV) is a major cause of cervical cancer globally. For early detection of premalignant dysplasia, evidences are coming out on the usefulness of HPV E6/E7 mRNA test as a potential tool compared with cytology and HPV DNA testing. Taking into account shortage of compiled data on this field, the aim of this systematic review.
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When either the HPV-8 early region, HPV-8 E6 or HPV-38 E6/E7 were expressed from a K14 promoter, this resulted in the formation of epidermal hyperplasia and, occasionally, squamous carcinomas. In addition, UV irradiation greatly increased the numbers of squamous cell carcinomas in these mice at levels that did not induce tumors in nontransgenic.