Overview: Conference on Early Cervical Neoplasia

Abstract

Department of Obstetrics and Gynecology, Mount Sinai School of Medicine, City University of New York, New York 10029 It is not clear to me that I am qualified to present the highlights of this interesting and important meeting, for as I listened to the discussion, it appeared to me that in some areas, I was underqualified and conversely in other areas, it would appear that I was overqualified. I stopped studying carcinoma of the cervix seriously 25 years ago because I came to the belief that the Pap smear would enable us to prevent death from this disease. I was almost right, but I was somewhat naive about the advancement of the behavioral sciences. In any case, we have not succeeded entirely, for we have not convinced a good segment of our population of the importance of periodic examination, nor have we succeeded nationwide in reaching the rural poor and the inner city high-risk patient. I believe this failure of total outreach to be a greater problem than that of frequency of screening. As in the case of cigarette smoking, we have not convinced the public of the virtue of our views about their health. The Chairman of the opening session offered some optimism in his suggestion that the newer technologies, including recombinant DNA methodology and hybridoma, would quicken the pace of the discovery of etiologic factors. Thereafter, we were warned by the next speaker against the unidimensional approach, considering the problems of tests for mutagenesis, tissue culture transformation, species specificity, and other genetic variation. The triad of host-agent-environment was invoked. We were cautioned against the interpretation of uncontrolled clinical studies, though some, such as those for cigarette smoking and lung cancer or analine dye and bladder cancer, pointed in the proper direction. In the case of cancer of the cervix the epidemiologic studies of coital factors led inexorably to herpes virus as the agent of choice, he stated. Following this introduction the next speaker stressed the importance of viral DNA in carcinogenesis with both Herpes Simplex virus and Papilloma virus related to genital diseases. The herpes virus was noted to be more complex with approximately 80 genes and known to be capable of causing chromosomal breaks, which incidentally, interferon could inhibit. The speaker informed us that Herpes Simplex virus II lodges in sacral root ganglia, S2-S4, and can be cyclically reactivated approximately four times yearly. It is known that this virus can transform cells in culture, and that these cells can cause tumors in animals.