Persistent Link:
http://hdl.handle.net/10150/604865
Title:
High-risk HPV: From Infection to Cervical Cancer Progression
Author:
Tseng, Roger Sean
Issue Date:
2015
Publisher:
The University of Arizona.
Rights:
Copyright © 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.
Abstract:
Human 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 [1]. 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 [65]. Specifically, the Sp1 binding site is conserved and necessary for VEGF and hTERT expression [65, 79].
Type:
text; Electronic Thesis
Keywords:
Cancer Biology
Degree Name:
M.S.
Degree Level:
masters
Degree Program:
Graduate College; Cancer Biology
Degree Grantor:
University of Arizona
Advisor:
Lantz, Robert C.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen
dc.titleHigh-risk HPV: From Infection to Cervical Cancer Progressionen_US
dc.creatorTseng, Roger Seanen
dc.contributor.authorTseng, Roger Seanen
dc.date.issued2015en
dc.publisherThe University of Arizona.en
dc.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.en
dc.description.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 [1]. 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 [65]. Specifically, the Sp1 binding site is conserved and necessary for VEGF and hTERT expression [65, 79].en
dc.typetexten
dc.typeElectronic Thesisen
dc.subjectCancer Biologyen
thesis.degree.nameM.S.en
thesis.degree.levelmastersen
thesis.degree.disciplineGraduate Collegeen
thesis.degree.disciplineCancer Biologyen
thesis.degree.grantorUniversity of Arizonaen
dc.contributor.advisorLantz, Robert C.en
dc.contributor.committeememberLantz, Robert C.en
dc.contributor.committeememberCampos, Samuel K.en
dc.contributor.committeememberLybarger, Lonnieen
All Items in UA Campus Repository are protected by copyright, with all rights reserved, unless otherwise indicated.