Abstract
The cervical squamocolumnar junction of normal and dysplastic human xenografts was maintained in SCID-beige mice. Dysplastic tissue maintained a dysplastic morphology, irregular pattern of keratin expression, elevated levels of cellular proliferation, and human papillomavirus type 16 and/or type 18 DNA. Hyperplastic changes of normal xenografts occurred via high-dose estrogen exposure, and through recombinant adenovirus infection, the introduction and stable expression of an exogenous gene was accomplished.
Highlights
Cancer of the uterine cervix is the most common cause of cancer-associated mortality in women worldwide [14]
Since over 90% of cervical malignancies are associated with infection by the high-risk human papillomavirus (HPV) subtypes (e.g., HPV 16 and 18) [2, 6], the ability to assess viral factors would be a prerequisite for the model
Working with transgenic mice expressing the HPV 16 oncoproteins E6 and/or E7, several investigators have elucidated molecular mechanisms associated with the induction of epidermal hyperplasia, angiogenesis, and DNA damage [19, 41, 42]
Summary
Cancer of the uterine cervix is the most common cause of cancer-associated mortality in women worldwide [14]. Since over 90% of cervical malignancies are associated with infection by the high-risk human papillomavirus (HPV) subtypes (e.g., HPV 16 and 18) [2, 6], the ability to assess viral factors would be a prerequisite for the model. The absence of the human cervical transformation zone and failure to support HPV cervical cancer-associated viral subtypes limit this model.
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