{"id":{"repo_id":"creighton","oai_identifier":"oai:cdr.creighton.edu:10504/55682"},"canonical_url":"https://search.dev.ndltd.org/etd/creighton/oai:cdr.creighton.edu:10504/55682","repository":{"repo_id":"creighton","name":"Creighton University","base_url":"https://cdr.creighton.edu/server/oai/request"},"display":{"title":"The Role of Erbb2 in Ultraviolet-Induced Nonmelanoma Skin Carcinogenesis","abstract":"Significance (from the introduction - no abstract provided) Nonmelanoma skin cancer is more common than all other forms of cancer combined and its incidence is increasing. Most of these cancers are caused by UV, which has many effects on the skin. The RTK Erbb2 is activated by UV and is overexpressed in some skin cancer. Targeted Erbb2 overexpression in a mouse model leads to spontaneous skin tumor development [82, 86, 87], However, the role of Erbb2 in the UV response of the skin and during UV-induced carcinogenesis is not known. We hypothesize that the UV-induced activation of Erbb2 increases skin tumorigenesis. To test this hypothesis and determine the mechanisms through which Erbb2 acts, the following specific aims were investigated: 1. Determine biological processes and downstream signaling modulated by Erbb2 in response to UV irradiation. (Chapter 2) 2. Determine the biological significance of Erbb2 activation during UV- induced tumorigenesis. (Chapter 3) 3. Determine the mechanisms through which Erbb2 enhances cell cycle progression following UV exposure. (Chapter 4) Through this research, we have demonstrated several important roles for Erbb2 during UV-induced skin carcinogenesis.","abstract_html":"Significance (from the introduction - no abstract provided) Nonmelanoma skin cancer is more common than all other forms of cancer combined and its incidence is increasing. Most of these cancers are caused by UV, which has many effects on the skin. The RTK Erbb2 is activated by UV and is overexpressed in some skin cancer. Targeted Erbb2 overexpression in a mouse model leads to spontaneous skin tumor development [82, 86, 87], However, the role of Erbb2 in the UV response of the skin and during UV-induced carcinogenesis is not known. We hypothesize that the UV-induced activation of Erbb2 increases skin tumorigenesis. To test this hypothesis and determine the mechanisms through which Erbb2 acts, the following specific aims were investigated: 1. Determine biological processes and downstream signaling modulated by Erbb2 in response to UV irradiation. (Chapter 2) 2. Determine the biological significance of Erbb2 activation during UV- induced tumorigenesis. (Chapter 3) 3. Determine the mechanisms through which Erbb2 enhances cell cycle progression following UV exposure. (Chapter 4) Through this research, we have demonstrated several important roles for Erbb2 during UV-induced skin carcinogenesis.","abstract_has_math":false,"creators":["Madson, Justin Gerhard"],"institution":"Creighton University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Hansen, Laura A."],"committee_chairs":[],"committee_members":[],"year":2006,"date_issued":"2006-06","date_published":"2006-06","updated_at":"2026-07-24T01:51:30Z","subjects":[],"languages":["en_US"],"rights":["Copyright is retained by the Author. A non-exclusive distribution right is granted to Creighton University and to ProQuest following the publishing model selected above."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10504/55682","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Hansen, Laura A."]},{"key":"dc:creator","label":"Author","values":["Madson, Justin Gerhard"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2014-06-17T13:31:24Z"]},{"key":"dc:date.issued","label":"Date","values":["2006-06"]},{"key":"dc:publisher","label":"Institution","values":["Creighton University"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_US"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright is retained by the Author. A non-exclusive distribution right is granted to Creighton University and to ProQuest following the publishing model selected above."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10504/55682"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Significance (from the introduction - no abstract provided) Nonmelanoma skin cancer is more common than all other forms of cancer combined and its incidence is increasing. Most of these cancers are caused by UV, which has many effects on the skin. The RTK Erbb2 is activated by UV and is overexpressed in some skin cancer. Targeted Erbb2 overexpression in a mouse model leads to spontaneous skin tumor development [82, 86, 87], However, the role of Erbb2 in the UV response of the skin and during UV-induced carcinogenesis is not known. We hypothesize that the UV-induced activation of Erbb2 increases skin tumorigenesis. To test this hypothesis and determine the mechanisms through which Erbb2 acts, the following specific aims were investigated: 1. Determine biological processes and downstream signaling modulated by Erbb2 in response to UV irradiation. (Chapter 2) 2. Determine the biological significance of Erbb2 activation during UV- induced tumorigenesis. (Chapter 3) 3. Determine the mechanisms through which Erbb2 enhances cell cycle progression following UV exposure. (Chapter 4) Through this research, we have demonstrated several important roles for Erbb2 during UV-induced skin carcinogenesis."]},{"key":"dc:title","label":"Title","values":["The Role of Erbb2 in Ultraviolet-Induced Nonmelanoma Skin Carcinogenesis"]}]}],"canonical_facts":{"dc:contributor.advisor":["Hansen, Laura A."],"dc:creator":["Madson, Justin Gerhard"],"dc:date.accessioned":["2014-06-17T13:31:24Z"],"dc:date.issued":["2006-06"],"dc:description.abstract":["Significance (from the introduction - no abstract provided) Nonmelanoma skin cancer is more common than all other forms of cancer combined and its incidence is increasing. Most of these cancers are caused by UV, which has many effects on the skin. The RTK Erbb2 is activated by UV and is overexpressed in some skin cancer. Targeted Erbb2 overexpression in a mouse model leads to spontaneous skin tumor development [82, 86, 87], However, the role of Erbb2 in the UV response of the skin and during UV-induced carcinogenesis is not known. We hypothesize that the UV-induced activation of Erbb2 increases skin tumorigenesis. To test this hypothesis and determine the mechanisms through which Erbb2 acts, the following specific aims were investigated: 1. Determine biological processes and downstream signaling modulated by Erbb2 in response to UV irradiation. (Chapter 2) 2. Determine the biological significance of Erbb2 activation during UV- induced tumorigenesis. (Chapter 3) 3. Determine the mechanisms through which Erbb2 enhances cell cycle progression following UV exposure. (Chapter 4) Through this research, we have demonstrated several important roles for Erbb2 during UV-induced skin carcinogenesis."],"dc:identifier.uri":["http://hdl.handle.net/10504/55682"],"dc:language.iso":["en_US"],"dc:publisher":["Creighton University"],"dc:rights":["Copyright is retained by the Author. A non-exclusive distribution right is granted to Creighton University and to ProQuest following the publishing model selected above."],"dc:title":["The Role of Erbb2 in Ultraviolet-Induced Nonmelanoma Skin Carcinogenesis"],"dc:type":["Dissertation"]},"updated_at":"2026-07-24T01:51:30Z"}