Reference SummaryMueller A, Cancer Res 1997 Dec 15;57(24):5542-9
Title |
A transgenic mouse model with cyclin D1 overexpression results in cell cycle, epidermal growth factor receptor, and p53 abnormalities. | ||||||
Authors |
Mueller A; Odze R; Jenkins TD; Shahsesfaei A; Nakagawa H; Inomoto T; Rustgi AK | ||||||
Journal |
Cancer Res | ||||||
Volume |
57 | ||||||
Issue |
24 | ||||||
Year |
1997 | ||||||
Pages |
5542-9 | ||||||
Abstract |
The cyclin D1 oncogene is critical in the progression of the cell cycle through the G1 phase. It is frequently overexpressed in squamous cell carcinomas originating from the head/neck and esophagus. Yet, the functional consequences of aberrant cyclin D1 overexpression are not entirely understood apart from increased cell proliferation. To address this question, we have developed a transgenic mouse model in which the EBV ED-L2 promoter targets cyclin D1 to the stratified squamous epithelium in a tissue-specific fashion to the tongue and esophagus, thereby resulting in a dysplastic phenotype. We now demonstrate that the dysplastic phenotype is associated with increased cell proliferation based on proliferating cell nuclear antigen overexpression and abnormalities in cyclin-dependent kinase 4, epidermal growth factor receptor, and p53. In aggregate, these studies suggest that alterations in certain oncogenes and tumor suppressor genes occur early during head/neck and esophageal carcinogenesis. | ||||||
Links |
J:45230 – MGI References 9407965 – National Library of Medicine/PubMed |
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Strain Notes
|
Strain | Model Name | Treatment Agent(s) | Organ Affected | Frequency | Model Details |
---|---|---|---|---|---|
FVB/N | Esophagus dysplasia | Esophagus |
0 |
||
FVB/N-Tg(L2hD)#Aru | Esophagus dysplasia | Esophagus |
100 |
||
FVB/N | Tongue dysplasia | Tongue |
0 |
||
FVB/N-Tg(L2hD)#Aru | Tongue dysplasia | Tongue |
100 |