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.