AuthorTseng, Roger Sean
AdvisorLantz, Robert C.
MetadataShow full item record
PublisherThe University of Arizona.
RightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
AbstractHuman papillomaviruses (HPV) are small non-enveloped viruses that infect basal cells. Most HPV infections are mild and develop warts at the site of infection. However, some high-risk serotypes of HPV are able to promote cancer formation. Serotypes 16 and 18 are responsible for the majority of cervical cancer cases . Its early proteins E6 and E7 promote oncogenesis by facilitating the acquisition of 7 hallmark traits necessary for cancer: constant signaling for proliferation, insensitivity to growth suppressors, evasion of apoptosis, limitless replicative potential, angiogenesis, immune evasion, and metastasis [1, 65, 68, 72, 76, 78, 79, 81, 82, 83, 84]. In addition to E6 and E7, specific conditions of an HPV infection seem to increase cancer incidence. Among these conditions are infection at the cervix's transformation zone, HPV genome integration with host chromosomes, inflammation and the presence of estrogen [1, 60, 61, 62, 63, 64, 69, 70, 71]. Estrogen's role in cervical cancer is not well understood. It is possible that it plays a role in the transcription of oncogenes by activating ERα and subsequently activating Sp1 . Specifically, the Sp1 binding site is conserved and necessary for VEGF and hTERT expression [65, 79].
Degree ProgramGraduate College