Cancer risk following treatment with non-contraceptive estrogens was studied in a population-based cohort of 23,244 women. Complete follow-up for an average of 6.7 years revealed 1,087 incident cancers versus 962.5 expected (relative risk/RR/ = 1.13; 95% confidence interval 1.10-1.20). We confirmed the recent findings of a more detailed analysis of the same cohort, based on a 1-year shorter follow-up period, namely: a markedly increased risk of endometrial cancer (RR = 1.8; 1.5-2.1), notably in women receiving potent estrogens, i.e., conjugated estrogens or estradiol (RR = 2.0; 1.6-2.4), and a slightly increased risk of breast cancer (RR = 1.1; 1.0-1.2). A slightly decreased risk of invasive cervical cancer (RR = 0.8; 0.5-1.2) is most likely due to more frequent smear taking than in the background population. There was no increase in the risk of cancer of ovary (RR = 1.0; 0.8-1.2), pancreas (RR = 0.8; 0.5-1.2), large bowel (RR = 1.0; 0.8-1.2) or kidney (RR = 1.0; 0.7-1.4). The risk of developing cancer in liver or biliary tract was lower than expected (RR = 0.4; 0.2-0.7), particularly in women who had used potent estrogens (RR = 0.3; 0.1-0.6), an unexpected finding which warrants further studies. Increased risks of malignant melanoma (RR = 1.5; 1.0-2.1) and lung cancer (RR = 1.3; 0.9-1.7) need cautious interpretation because of their low magnitude, the absence of a biological gradient when subgroups were analyzed and the slightly higher prevalence of smokers in the cohort than in the background population.

By linking HIV/AIDS and cancer surveillance data in 12 US regions, breast and reproductive cancer risks with AIDS were compared to those in the general population. Trends in standardized incidence ratios (SIRs) were assessed by CD4 count, AIDS-relative time, and calendar time. Standardized incidence ratios were indirectly adjusted for cancer risk factors using data from AIDS cohort participants and the general population. With AIDS, 313 women developed breast cancer (SIR 0.69, 95% confidence interval (CI) 0.62 -0.77), 42 developed ovary cancer (SIR 1.05, 95% CI, 0.75 -1.42), and 31 developed uterine corpus cancer (SIR 0.57, 95% CI, 0.39 -0.81). Uterine cancer risk was reduced significantly after age 50 (SIR 0.33). Breast cancer risk was reduced significantly both before (SIR 0.71) and after (SIR 0.66) age 50, and was lower for local or regional (SIR 0.54) than distant (SIR 0.89) disease. Breast cancer risk varied little by CD4 count (P trend ¼ 0.47) or AIDS-relative time (P trend ¼ 0.14) or after adjustment for established cancer risk factors. However, it increased significantly between 1980 and 2002 (P trend ¼ 0.003), approaching the risk of the general population. We conclude that the cancer deficit reflected direct or indirect effects of HIV/AIDS and that anti-HIV therapy reduced these effects. Increasing numbers of women have been infected with human immunodeficiency virus (HIV) and now are living with the acquired immunodeficiency syndrome (AIDS). The effects of AIDS on women, particularly in the era of highly active antiretroviral therapy (HAART), are not well defined. In the era before HAART, the risks of developing Kaposi sarcoma, anal cancer, and perhaps lymphoma were lower for women than for men with AIDS (Beral and Newton, 1998;Goedert, 2000). Other than cervical cancer, no differences by gender have been reported for the few other malignancies found in excess among people with AIDS (PWA) (Goedert et al, 1998;Frisch et al, 2001).Breast cancer may occur less often in women with AIDS than in the general population (Goedert et al, 1998;Frisch et al, 2001). Ovary and uterine corpus cancers have not been associated with AIDS or other immune deficiencies, but weak associations or susceptible subgroups may have been overlooked because these malignancies are relatively rare. No previous study has evaluated the effects of improving anti-HIV therapies or whether differences in cancer incidence might merely reflect differences in known risk factors for cancer.Using population-based data, we have investigated whether the risk of breast, ovary, or uterine corpus cancers differ for women with AIDS, whether breast cancer risk differs with increasing severity or duration of immune deficiency, or with increasing availability and efficacy of anti-HIV therapies; also whether menopause or selected risk factors modify or explain any associations. MATERIALS AND METHODS Detection and definition of cancersFrom 2003 through 2005, we linked HIV/AIDS and cancer registration data (including name, race, sex, dates of birth and de...

High levels of serum estrogens and androgens have been convincingly linked with an increased risk of breast cancer among postmenopausal women. By contrast, the role of blood levels of these hormones in the etiology of premenopausal breast cancer is not well understood. In a case-control study, we sought to examine associations between levels of serum estradiol, sex-hormone binding globulin (SHBG), dehydroepiandrosterone (DHEA), testosterone, androstenedione and progesterone and risk of premenopausal breast cancer. Cases of breast cancer under age 45 were identified using rapid ascertainment systems in Seattle/Puget Sound, Washington and control subjects were identified from the same area through random digit dialing methods. A total of 169 eligible breast cancer cases and 195 control subjects donated blood (either before or six or more weeks after surgery) and were interviewed using a standardized questionnaire. The fully adjusted risk ratios and 95% confidence intervals for the highest versus lowest tertiles of estradiol, according to menstrual cycle phase, were 3.10 (0.8-12.7) for early follicular, 0.54 (0.2-1.7) for late follicular and 0.60 (0.3-1.4) for luteal. Risks for highest versus lowest quartiles of SHBG and androgens were 0.81 (0.4-1.6) for SHBG, 2.42 (1.1-5.2) for DHEA, 1.12 (0.6-2.5) for testosterone, and 1.33 (0.6-2.8) for androstenedione. For luteal progesterone, the RR for the highest versus lowest tertile was 0.55 (0.2-1.4). In summary, we did not find a convincing association between serum SHBG, estradiol, testosterone or androstenedione and premenopausal breast cancer risk. Observed differences between cases and controls subjects in serum levels of DHEA and luteal phase progesterone should be investigated further in large prospective studies.

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