Chapter 24. Analyzing Cervical Cancer Through Mouse Models
Introduction
Analyze the Data
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Analyze the Data 24-2: Analyzing Cervical Cancer Through Mouse Models
The E7 oncoprotein of the high-risk human papillomaviruses (HPV) is thought to contribute to cervical carcinogenesis at least in part by disrupting regulation of the cell cycle in cervical epithelial cells. E7 can misregulate the cell cycle through its interaction with several cellular proteins, including the retinoblastoma suppressor protein RB as well as the cyclin-dependent kinase inhibitor p21Cip1.
Question
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_feedback: Transgenic models can be utilized to either enhance p21 (+/+) mice or eliminate p21 (–/–) expression of certain proteins. Mutant viral proteins, including E7, can be expressed in transgenic mouse models to isolate the function of these proteins from that of normal cellular proteins. This can help to establish causal relationships between the mutations and alterations in normal cellular phenotypes, including oncogenesis.
Question
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_feedback: This would support a loss-of-function role for p21 because this suggests that expression of p21 may have a positive impact on tumor-suppressor activity in the cell.
Question
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_feedback: Yes this would be consistent with the hypothesis—if E7 expression did not inhibit p21, then its tumor-promoting activity would be enhanced in the p21-null background relative to the p21 (+/+) background.
Question
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_feedback: E7 expression vectors can be constructed ex vivo and then utilized to trans-form cell types of interest or in animal models of cervical cancer. These expression vectors can include E7 mutations of interest.
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