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Effects of oral contraception on neoplasia of the uterine corpus are reviewed on the basis of epidemiologic studies reported to date. A duration-related protective effect against endometrial cancer occurs from use of combined oral contraceptives, those in which each active pill contains both estrogen and progestogen. The risk before age 60 years is reduced by about 38% with two years of use; use of combined OCs for 4, 8, and 12 years, respectively, confers an estimated 51%, 64%, and 70% reduction in endometrial cancer risk. The protective effect appears not to be diminished by discontinued use, even 15 or more years after stopping. Whether protection continues throughout the entire postmenopausal period, even in the presence of long-term hormone replacement therapy, remains to be seen. Use of combined OCs may protect against uterine leiomyomas ("fibroids"), but the evidence is not conclusive. The few findings about effects of oral contraception on the risk of adenomatous hyperplasia are of uncertain validity. Only one study, with few patients, has considered oral contraception in relation to uterine sarcomas.

A long-term effect of oral contraceptives (OCs) on breast cancer risk has been suggested as an explanation for some studies' failure to detect an association between OCs and breast cancer. To address this latency hypothesis, we analyzed data on 4714 case subjects and 4540 control subjects from the population-based Cancer and Steroid Hormone Study. No support was evident for a latent effect of OCs on breast cancer risk through age 54 years: among parous women who had cumulated more than six years of OC use before their first term pregnancy, the risk of breast cancer, relative to nonusers before first term pregnancy, was 0.6 at zero to four years after first term pregnancy (95% confidence interval [Cl], 0.2 to 1.8), 0.7 at five to nine years (95% Cl, 0.3 to 1.7), and 1.1 at ten to 14 years (95% Cl, 0.3 to 3.9). Among nulliparous women with more than six years of OC use in total, the relative risk of breast cancer, by interval from last use of OCs, was 1.3 at zero to four years (95% Cl, 0.8 to 2.0), 1.1 at five to nine years (95% Cl, 0.5 to 2.0), and 0.6 at ten to 14 years (95% Cl, 0.1 to 3.7).

We report analyses designed to address the recent hypothesis that women who use combination-type OCs containing ethinylestradiol (EE) are at increased risk of breast cancer before age 45, if use of such OCs occurs prior to first term pregnancy (FTP). Our findings, based on data from 1679 cases and 1689 controls, 20-44 years of age, from the population-based Cancer and Steroid Hormone Study, are against the hypothesis. The relative risk of breast cancer by duration of exclusive use prior to FTP of OCs containing EE is estimated to be 1.0 (1-12 months EE use), 1.2 (13-48 months EE use), and 0.9 (49+ months EE use). There was no evidence of a latent effect. Among parous women with 49+ months exclusive use prior to FTP of EE-containing OCs, the relative risk of breast cancer was estimated as 0.9 (0-4 years after FTP) and 0.6 (5-9 years after FTP). Among nulliparous women with 49+ months exclusive use of EE-containing OCs, the relative risk of breast cancer was estimated as 1.0 (0-4 years since first use), 0.7 (5-9 years since first use), and 1.1 (10-14 years since first use). With regard to exclusive use of OCs containing mestranol, parous women who used such preparations long-term before their FTP showed no alteration of breast cancer risk, even 15 years or more after pregnancy. Nulliparous women with exclusive use of ME-containing OCs did show elevations in breast cancer risk, but the magnitude of risk in relation to duration of use and latent interval shows no pattern that suggests a cause-effect relationship.