婦人科細胞診の理論と実際

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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-defferentiation. In histology, however, differentiated cells are thought to be normal cells from the histological definition. Therefore, the hisological 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 prolifirate 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 degradiation 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 transfered 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. Step I, early stage, is dyskeratosis and nuclear enlargements of intermediate cells. Step II, middle stage, is the increasing of binucleated cells from intermediate layer to upper layer, small number of parabasal cells with dyskaryosis, and giant cell formation. Stap III, late stage, is binucleation, multinucleation, karyorrhexis, bizzare-cells, and many other findings of parabasal cells. Step III include two important findings. 1. appearance of small cells, 10-15μm in diameter 2. appearance of a cluster of small hyperchromatic cells Finally, we should discriminate small cells identified as cancer cells, from differentiated dyskaryotic cell. And the stage of dysplasia should not be decided by the degree of cell differetiation from low layer to upper layer, but by the careful observation on the abnomal cells from upper layer to lower layer.
社団法人日本産科婦人科学会の論文
1994-08-01

婦人科細胞診の理論と実際

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