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Verh Dtsch Ges Pathol. 1997;81:240-4.

Histopathology of functional and neoplastic changes in cervix and endometrium.

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Institut für Pathologie, Mannheim.


Over 90% of all cervical carcinomas originate from hyperplastic reserve cells of the endocervix. When cell cycles of the pluripotent reserve cells are shortened or damaged by hormonal overstimulation or toxic chemicals, DNA repair after viral infection is no longer possible. The immortalized cells may then become malignant with precancerous and carcinomatous differentiation to squamous, adenosquamous or adenocarcinomas. To determine the type of HPV infection is clinically important for estimating prognosis and for planning further therapy. In recent years HPV 18-associated endocervical adenocarcinomas have increased considerably in number as compared with squamous cell carcinomas. In endometrial carcinomas the estrogen-stimulated endometrioid types must be distinguished from the gestagen-stimulated mucinous, clear-cell and serous-papillary types because prognosis as well as operative and adjuvant therapy differ considerably. The endometrioid carcinomas and their preceeding atypical hyperplasia are frequently associated with bcl-2, c-myk and c-ki-ras oncogenes. The mixed Muellerian types, in contrast, and their preceeding mucinous, clear-cell and serous-papillary metaplasias very often show genetic defects, LOH, mutations, amplifications and deletions, especially of p53. The endometrial carcinomas occurring in the reproductive age period are of endometrioid type and frequently present microsatellite instabilities. In rapidly proliferating tissues like the endometrium there appears to be a close correlation between functional and neoplastic changes. A simple explanation for that might be found in the greatly enhanced mitotic activity in a hormonally stimulated endometrium with shortening of cell cycles, leaving insufficient time for DNA repair. Since, however, carcinogenesis is a multi-factorial event, to correlate endometrial function with morphology can contribute only one aspect to the understanding of neoplastic change. In discussing hormonal function it is important to realize that the endocervix and the endometrium differ not only in their cellular structure, but they react antagonistically to hormonal stimulation: excessive (endogenous or exogenous) estrogen results in hyperproliferation of endometrial epithelial cells, but in the cervix in differentiation of the endocervical cells with mucus production. Extensive synthetic gestagens lead to hyperproliferation of endocervical epithelial cells (reserve cells as well as glandular epithelial cells), but in the endometrium cause atrophy (see Table 1).

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