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Data from a population-based case-control study of chronic lymphocytic leukemia were analyzed to assess the possible etiologic role of chronic antigenic stimulation. The study, conducted in four geographic areas of the United States (the metropolitan areas surrounding Seattle, Washington, Salt Lake City, Utah, Detroit, Michigan, and Atlanta, Georgia) sought to identify all incident cases (n = 430) among residents diagnosed between July 1, 1977 and December 31, 1981. The responses of these cases to questions about possible sources of antigenic stimulation were compared with the responses of controls selected from the populations of these areas. Little difference between cases and controls was present for a history of most forms of viral and bacterial infection and for a history of allergies or allergy treatment. However, a relation was observed with antecedent syphilis infection (odds ratio (OR) = 5.0, 95% confidence interval (Cl) 2.0-12.9). Associations of smaller magnitude were observed with a history of tuberculosis (OR = 1.9, 95% Cl 1.0-3.7) and of urinary tract infection (OR = 1.4, 95% Cl 1.1-1.9). Overall, however, the authors found little evidence of a relation between chronic antigenic stimulation and the occurrence of chronic lymphocytic leukemia. Nonetheless, because the measure of prior antigenic stimulation was restricted to that obtained through interviews and undoubtedly was an insensitive one, these negative results should not be interpreted as ruling out antigenic stimulation as a possible cause of some cases of chronic lymphocytic leukemia.

Female residents of six counties in Washington and Utah in whom a diagnosis of ovarian cancer was made during 1975-79 were interviewed concerning prior use of oral contraceptives. Interviews with a random sample of women drawn from these same counties were obtained for comparison. A smaller proportion of women with epithelial ovarian tumors had taken oral contraceptives than had controls: the estimated risk of ovarian cancer in uses relative to that in non-users was 0.57 (p = 0.04). The magnitude of the decreased risk depended on the duration over which oral contraceptives had been taken, as the negative association was present only after 4 or more years of use. In many ways, the use of oral contraceptives mimics the physiologic effects of pregnancy. The results of the present investigation, when interpreted together with those from other epidemiologic studies and from experiments in animals, suggest that, like pregnancy, the use of oral contraceptives has a protective effect against the development of ovarian cancer.

Female residents of six counties in Washington and Utah in whom ovarian cancer was diagnosed during 1975-79 were interviewed concerning prior use of noncontraceptive estrogens. Interviews with a random sample of women drawn from these counties were obtained for comparison. Taken as a whole, women with epithelial ovarian tumors reported estrogen use for 1 year or more somewhat more often than did controls [relative risk (RR) = 1.3, 95% confidence interval (CL) = 0.9-1.8]. The proportion of women who had used estrogens varied according to the histology of their tumor; notably, of 17 women with endometrioid tumors, 12 had used estrogens (RR = 3.1, 95% CL = 1.0-9.8). The excess risk of endometrioid carcinoma related to estrogen use was not further increased when these hormones were taken for long durations, in high doses, or proximate to the time of diagnosis. Neither was there any evidence of increased risk from estrogen use in the small group of women with clear cell tumors, a histologic tumor type believed to be closely related to endometrioid carcinoma. Thus the observed association between menopausal estrogen use and the occurrence of ovarian endometrioid tumors should be interpreted cautiously until the results of additional studies are available.

Women resident in six counties of Washington and Utah for whom diagnoses of epithelial ovarian cancer were made during 1975-1979 were interviewed concerning their menstrual, reproductive and medical histories. For comparison, interviews were also obtained from a random sample of women living in the same countries. Logistic regression methods were used, and histories of childbearing, miscarriages, lactation, and (in Washington) usage of oral contraceptives were found to be associated with decreased risk of ovarian cancer; the estimated relative risks were, respectively, 0.88 per pregnancy (i.e., 0.88(2) for two pregnancies, etc.) (p = 0.016), 0.82 per miscarriage (p = 0.049), 0.79 per year of lactation (p = 0.034), and 0.89 per year of oral contraception (p = 0.009). In addition, it was observed that the magnitudes of the diminished risks from these exposures substantially exceeded those which would have been expected solely on the basis of their inhibition of ovulation (X2(5) = 21.5, p = 0.0006). On the other hand, the lack of association found between the occurrence of ovarian cancer and either total dose or total time of exposure to noncontraceptive estrogens, or with a history of usage of thyroid medications, suggests that periods of reduced pituitary gonadotrophin secretion fail to reduce risk of ovarian cancer. Thus, although pregnancy, lactation and oral contraception appear to offer some protection against the development of epithelial ovarian cancer, the reasons remain obscure.