作者: Theodoros Rampias , Amanda Psyrri
DOI: 10.1007/978-1-4614-8815-6_11
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摘要: All known human papillomaviruses (HPVs) are exclusively epitheliotropic. Upon entry into populations of stratified epithelial cells, the E6 and E7 oncoproteins encoded by high-risk HPV variants establish a productive infection manipulating signaling processes in host environment, leading ultimately to production infectious particles upper layers. The mechanisms which promote cell-cycle progression viral DNA replication well established, involve E6-dependent ubiquitination degradation p53 tumor suppressor, E7- cullin 2-dependent retinoblastoma (Rb) suppressor protein. Recent experimental work provides evidence that HPVs also manipulate underlying differentiation status cells targeting Wnt pathway ensure cycle. This chapter summarizes possible cell pathways involved activation HPV-positive head neck cancer.