[Gynecological cytology in theory and practice]

The points of this presentation are reform of the theory relating to "Dysplasia and Carcinogenesis" and the cytological methods. In 1976, Meisels and Fortin reported that dysplasia is the disease caused by Human papilloma virus (HPV), and surprisingly, intermediate cells infected by HPV possessed the ability of proliferation and mitosis, resulting in binucleation and multinucleation. In cytology, dysplasia is thought to be delivered from basal cells and abnormal cells are differentiated from lower layer to upper layer, the grade of dysplasia is judged from the level of cell-differentiation. In histology, however, differentiated cells are thought to be normal cells from the histological definition. Therefore, the histological theory cannot explain the fact that the appearance of the abnormal cells from the all layers in cytology of the mild dysplasia. This discrepancy can be understood well if we think it is caused by HPV infection. HPV (ds-DNA) can only proliferate using cellular factors. And as keratinocytes is important with relating to this proliferation, HPV affects human intermediate layer and upper layer. In HPV-infected cells, HPV-E6 protein and E7 protein can bind the products of p53 and pRB, suppressor genes, respectively. These lead to degradation of these proteins' function, acceleration of cell proliferation, and abnormality of cell-cycle time. Our fundamental theory of dyskaryosis is based on these findings. Mild dysplasia is transferred from intermediate layer to upper layer and vanish after cell maturation. Immortalization, transformation, and gene alteration are important factors for carcinogenesis. The deletion of chromosome 3p is one of the most important genetic changes during carcinogenesis. On the basis of carcinogenesis theory described above, the cytological findings of HPV-infected cells are classified into three steps.(ABSTRACT TRUNCATED AT 250 WORDS)