作者: R Herber , A Liem , H Pitot , P F Lambert
DOI: 10.1128/JVI.70.3.1873-1881.1996
关键词: Papillomavirus E7 Proteins 、 Keratin 、 Transgene 、 Cellular differentiation 、 Carcinogenesis 、 Immunology 、 Cancer research 、 Biology 、 Papillomaviridae 、 Hyperplasia 、 Oncogene
摘要: The human papillomavirus type 16 (HPV-16) genome is commonly present in cervical carcinoma, which a subset of the viral genes, E6 and E7, are expressed. HPV-16 E7 gene products can associated with inactivate tumor suppressor proteins p53 Rb (the retinoblastoma susceptibility product), tissue culture cells, these genes display oncogenic properties. These findings have led to hypothesis that contribute carcinogenesis. This has recently been tested by using transgenic mice as an animal model. together were found induce cancers multiple tissues they expressed, including squamous cell cancer most cervix. We extended studies investigate vivo activities when expressed epithelia mice. Grossly, had phenotypes, wrinkled skin was apparent prior appearance hair on neonates, thickened ears, loss adults. In lines expressing higher levels we observed stunted growth mortality at early age, potentially caused incapacity feed. Histological analysis demonstrated causes epidermal hyperplasia lineages high penetrance. epithelial characterized expansion proliferating compartment keratin 10-positive layer cells hyperkeratosis. Hyperplasia sites animals addition skin, mouth palate, esophagus, forestomach, exocervix. lineages, adult developed tumors late life low arose from sebaceous glands histologically be highly differentiated, locally invasive, aggressive their On basis conclude alter parameters sufficiently potentiate tumorigenesis