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• W2096325004 abstract "Summary With various human clinical, epidemiological, and ex perimental data together with basic carcinogenesis ex perimentation, a working hypothesis of the development of cervical cancer is presented. Initiation may involve a carcinogen (perhaps herpesvirus type 2) altering the sus ceptible metaplastic cervical cell that is active in adoles cence and during pregnancy. Promotion by factors per haps related to coitus or to the continued metaplastic process in a field of abnormally mitosing cells allows for selection of a clone of cells with the characteristics of un limited growth and invasion. Human cervical cancer and its antecedent lesions (dysplasia and CIS2) offer a unique opportunity to study the pathogenesis of a human neoplasm. The cervix is a com mon site of neoplastic change, it is readily accessible so that preinvasive lesions may be accurately diagnosed, and there is a wealth of epidemiological and experimental data relating to the spectrum of this disease. The recent ex periments exploring the possible association of herpes simplex virus type 2 and cervical cancer must be applied to the wealth of clinical and experimental data on cervical cancer, CIS, and dysplasia. The opening session of the Symposium on Herpesvirus and Cervical Cancer was designed to acquaint the participants with some of the ex perimental studies and theories related to the develop ment and progress of cervical cancer. This paper is an attempt to utilize some of these experimental data to develop a working hypothesis that may be useful in ex plaining the relationship between dysplasia, CIS, and in vasive cervical carcinoma. This relationship between the various phases in the spectrum of cervical neoplasia may allow a more intelligent speculation and hopefully may be followed by the investigation of the mechanism that the herpesvirus might have in relation to the disease." @default.
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• W2096325004 date "1973-06-01" @default.
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• W2096325004 title "A selective review of experimental studies in cervical carcinoma." @default.
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