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Query: UMLS:C0006142 (breast cancer)
160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The new generation of oral contraceptives (OCs) contains less than 50 mcg of estrogen compared to previous levels of 100-150 mcg, and as a result have fewer undesirable side effects. In addition, it appears that the newer OCs decrease the susceptibility to many diseases. For example, the pill decreases by 40% the risk that a woman under 55 years of age will develop ovarian cancer. The risk of endometrial cancer is reduced by 50% in OC users. The pill also significantly lowers the risk of pelvic inflammatory disease--a condition that is involved in almost 20% of all gynecologic problems and is a leading cause of infertility. OC use reduces the risk of ectopic pregnancy. Further, by decreasing menstrual blood flow, the pill protects against iron-deficiency anemia. The pill is claimed to decrease premenstrual tension, menstrual cramps, and even acne. It has a protective effect against ovarian cysts and benign breast cancer. Finally, there is the possibility that OCs protect against the development of rheumatoid arthritis and duodenal ulcers.
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PMID:Oral contraceptives come of age. 385 23

Between January 1980 and March 1983, data were collected to evaluate risk factors for breast cancer in a case-control study based on 368 women with breast cancer admitted to the General Hospital of Pordenone (a district in North Eastern Italy with a particularly high breast cancer mortality rate), and 373 age-matched controls. Nulliparity or low parity, late age at first birth and later menopause were associated with an increased risk of breast cancer. The elevated risk associated with nulliparity could be almost completely explained by marital status, thus pointing to a specific protection given by parity, rather than some putative influence of infertility or subfertility in breast cancer cases. Likewise, risk did not vary materially according to history of abortions when marital status was controlled for. Increased risk associated with later age at first birth, on the other hand, was not accounted for by marital status or parity. The population studied, though frequently multiparous, showed late average at first birth: this might, at least partly, explain its high mortality rate from breast cancer. The risk estimate was higher if menarche occurred below age 15; however, there was no evidence of a trend for the relative risk to rise with lower age at menarche. The use of oral contraceptives or other female hormones (such as oestrogen replacement therapy) did not appear to be related to the risk of breast cancer. The role of the major menstrual and reproductive variables considered (age at menarche, parity, age at first birth) was apparently stronger in pre-menopausal women, thus suggesting an influence of these factors (and possibly, their hormonal correlates) on one of the latter stages of the process of carcinogenesis.
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PMID:Reproductive and hormonal factors and breast cancer in a Northern Italian population. 398 43

To clarify the role of marital status in human carcinogenesis, a 1968 Cancer Institute study analyzed the cancer mortality experience of 31,658 white Catholic nuns from 41 religious orders in the U.S. from 1900-1954. The national white female population was used for cause-specific comparison and both groups were assigned cohorts depending upon the year of birth. When examined by 10-year age groups, rates for cancer at all sites was generally lower for nuns than for controls aged 59 or 69 but were substantially higher at older ages. Postmenopausal nuns (aged 69 and over) displayed a higher rate (38.6%) of cancer of the large intestine than did controls (22.6%) but had a lower proportion of deaths from cancer of the biliary passages and liver (13.0% vs. 22.6%). Nuns displayed a striking excess in breast cancer mortality over the age span of 40-74 years and had consistently higher rates than controls for each age group above 39 years. Lower cervical cancer rates for nuns (10.8%) than for controls (56.6%) seemed related to coital factors. Cancer of the uterus accounted for 63% of the genital cancer deaths among sisters. Overall, the genital cancer mortality rates for nuns were consistent with high mortality rates for the single, white female population of the U.S. The increased risk of breast cancer and cancers of the corpus uteri and ovary would seem to reflect an established link with infertility. Combination of these factors with the excess incidence of cancer of the large intestine among postmenopausal nuns suggests a common pathogenic mechanism of a hormonal nature operating in some women.
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PMID:Cancer mortality among nuns: role of marital status in etiology of neoplastic disease in women. 577 91

The effect of smoking on the development of breast, endometrial, and ovarian cancers is evaluated among cases identified between November 1980 and July 1982 in the Iowa Surveillance, Epidemiology, and End Results Cancer Registry. Population-based, age-frequency matched controls were also evaluated, adjusting for potential confounders: Age, age of menarche, age of menopause, duration of menses, female family reproductive cancer history, obesity, parity, infertility, and lifetime steroid hormone use. Logistic regression analyses of total pack-years of cigarette exposure indicate that smoking is not significantly related to the development of breast cancer [relative risk (RR) = .99; confidence interval (CI) = .97, 1.02] or ovarian cancer (RR = 1.00; CI = 1.00, 1.00). Among women with endometrial cancer, the risk for those who smoke is increased among premenopausal women (RR = 1.27; CI = .65, 2.59) and decreased among postmenopausal women (RR = .41; CI = .16, 1.04).
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PMID:Effects of smoking on the development of female reproductive cancers. 658 29

Estrogens, whether natural or synthetic, have a wide range of clinical uses in the human female. In prepubertal females, estrogens are used in treating gonadal dysgenesis, excessive height, and genital infections. During the reproductive years, estrogens are used in managing 1) menstrual disorders (amenorrhea, menorrhagia, dysmenorrhea); 2) infertility (poor cervical mucus and anovulation); 3) pregnancy (abortion, lactation suppression); 4) dermatological disorders (acne vulgaris, hirsutism); 5) combined estrogen/progestogen usage for contraception; and 6) postcoital contraception. During the climacteric/postmenopausal years, estrogens are used in treating menopausal syndrome and breast cancer as well as various genital problems (infection, atropic vaginitis, genital prolapse). In the human male, estrogens are used in treating prostatic carcinoma and sexual problems. Estrogen therapy should be used with caution, and benefits should be weighed against the hazards. Possible side effects and alternative forms of treatment should be considered.
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PMID:Clinical uses of estrogens. 700 4

In order to investigate the nature of the association of involuntarily delayed 1st birth and breast cancer risk, 1083 white women who had been evaluated and treated for in fertility from 1945-65 were followed prospectively through April 1978 to ascertain their breast cancer incidence. These women were categorized as to the cause of infertility into 2 groups, those with endogenous progesterone deficiency (PD) and those with nonhormonal causes (NH). Women in the PD group had 5.4 times the risk of premenopausal breast cancer as compared to women in the NH group. This excess risk could not be explained by differences between the 2 groups in age at menarche or age at menopause, history of oral contraceptive use, history of benign breast dieases, or age at 1st birth. Women in the PD group also experienced a 10-fold increase in deaths from all malignant neoplasm compared to the NH group. The incidence of postmenopausal breast cancer did not differ significantly between the 2 groups.
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PMID:Breast cancer incidence in women with a history of progesterone deficiency. 730 56

Case-control studies are reported of 1868 breast cancer patients and 3391 unaffected women from the San Francisco Bay Area that identify clues to the etiology of breast cancer and distinguish characteristics of patients with premenopausal, paramenopausal, or postmenopausal dates of 1st diagnosis. Patients with breast cancer diagnosed during 1970-1977 were interviewed at home, as were twice as many control patients from the same hospitals matched to the cancer patients by age (within 5 years), race (white or black), and time of hospitalization (within 7 months). Rates of participation through interview were about 70%, somewhat higher for breast patients than for control patients. Common to increased risk of breast cancer in periods of womanhood were: early menarche and late menopause; delayed marriage and 1st childbirth; more nulliparity or reduced gravidity and parity; reduced frequency of abortions; shorter overall childbearing interval; more advanced education, higher socioeconomic status, and more contraceptive usage; and familial tendencies toward the disease. Breast cancer patients diagnosed before menopause were leaner than controls at age 20 and at time of diagnosis, but breast cancer risk in the postmenopausal period was related to increased weight-for-height at diagnosis and greater weight gain since age 20. Postmenopausal breast cancer patients had a longer interval between 1st and 2nd childbirths. Frequency and duration of the gravid state, inversely related to breast cancer risk, were largely dependent on contraceptive practices rather than unexplained infertility per se. Whether the breast cancer reaches diagnosis before or following menopause, the bulk of the evidence examined supports the view that it has a common cause and is subject to modifying influences over the long period of cancer latency.
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PMID:Characteristics that predict risk of breast cancer before and after the menopause. 741 52

Concern has been expressed that exposure to fertility drugs might be associated with a risk of ovarian cancer. We have examined the incidence of breast and ovarian cancer in a cohort of 10,358 women referred for in-vitro fertilisation (IVF) treatment in Victoria, Australia, between 1978 and 1992. The "exposed" group (n = 5564) had had ovarian stimulation to induce multiple folliculogenesis and the "unexposed" group (n = 4794) had been referred for IVF but were untreated or had had "natural cycle" treatment without ovarian stimulation. Duration of follow-up ranged from 1 to 15 years. Cases of cancer were determined by record linkage with data from population-based cancer registries. 34 cases of invasive breast cancer and 6 of invasive ovarian cancer were observed. A comparison with the expected numbers, derived by applying age-standardised general population rates to the cohort gave standardised incidence ratios (SIR) for breast cancer of 0.89 (95% CI 0.55-1.46) in the exposed group and 0.98 (0.62-1.56) in the unexposed group, and for ovarian cancer SIRs were 1.70 (0.55-5.27) and 1.62 (0.52-5.02), respectively. Rates of all cancers were not significantly different from general population rates. The relative risk (RR) of cancer, adjusted for age and infertility type, was, in the treated group compared with the untreated group, 1.11 (95% CI 0.56-2.20) for breast cancer and 1.45 (0.28-7.55) for ovarian cancer. The risk of body of uterus cancer was increased in the exposed and unexposed groups combined (SIR 2.84 [1.18-6.81]). Women with unexplained infertility, independent of IVF exposure, had significantly increased risks of ovarian cancer (RR = 19.19 [2.23-165.0]) and body of uterus cancer (RR = 6.34 [1.06-38.0]) compared with women with known causes of infertility. This relatively short-term follow-up suggests that ovarian stimulation with IVF is not associated with an increased risk of breast cancer. Although there was no significantly increased risk of ovarian cancer after ovarian stimulation with IVF the small number of cases limits the conclusions that can be drawn. Longer-term follow-up of large cohorts of women who have been in IVF programmes will be necessary.
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PMID:Breast and ovarian cancer incidence after infertility and in vitro fertilisation. 750 Jul 68

Studies of the induction of mammary tumors by 7,12-dimethylbenz(a)anthracene in a rat model show that human chorionic gonadotropin (hCG) administration reduces tumor incidence in a manner comparable to that of a completed pregnancy. On the basis of their studies, Russo and Russo (Cancer Epidemiol., Biomarkers & Prev., 3: 353-364, 1994) have proposed that hCG treatment of young nulliparous women would reduce their breast cancer risk in a manner similar to that of a term pregnancy. As part of a population-based, case-control study of breast cancer among women ages 40 years or younger, we asked women whether they had received hCG injection as part of a weight loss regimen or as a component of infertility treatment. Participants in this study were 744 women newly diagnosed with breast cancer between July 1983 and December 1988 and 744 controls individually matched on birthdate (within 36 months), race (white), parity (nulliparous/parous), and neighborhood of residence. Forty-five cases and 65 controls reported exposure to hCG (multivariate odds ratio = 0.77, 95% confidence interval = 0.50-1.19). Risk was reduced significantly among women whose maximum nonpregnant body mass index was less than 27.5 kg/m2 but no reduction in risk was observed among more obese women. Although the odds ratios were reduced substantially for both nulliparous and parous women with maximum nonpregnant body mass indices less than 27.5, only the result for nulliparous women was statistically significant. These results are consistent with the effects proposed by Russo and Russo based on their animal model. Although not definitive, these results suggest that hCG may be a means for reducing breast cancer risk.
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PMID:Treatment with human chorionic gonadotropin and risk of breast cancer. 754 96

Dietary phytoestrogens have been implicated in infertility among ruminants and may relate to human breast cancer risk. Formononetin is an isoflavonoid phytoestrogen found in animal fodder and in certain human foodstuffs. To investigate a possible mechanism by which phytoestrogens might influence mammary carcinogenesis, this study examined the capacity of formononetin to stimulate mammary gland proliferation. Formononetin was administered to castrated female BALB/c mice by daily subcutaneous injection; then mammary gland proliferation and estrogen receptor expression were quantified, and plasma prolactin levels were measured. A preliminary dose-finding study demonstrated an estrogenic effect on vaginal cytology when formononetin was injected at 40 mg/kg sc. Peak plasma concentrations of 2.5 +/- 0.8 (SD) micrograms/ml at two hours and peak mammary tissue concentrations of 2.0 +/- 0.2 ng/mg tissue at four hours were noted after a single injection at this minimally bioactive dose. Among animals treated with formononetin at 40 mg/kg/day for five days, mammary gland proliferation was enhanced 3.3-fold over saline-treated controls and was comparable to that of animals treated with estradiol-17 beta at 1 microgram/kg/day for five days. Mammary tissue estrogen receptor expression was 2-fold higher among the formononetin-treated animals (P < 0.01 vs. saline-treated controls), and plasma prolactin concentrations were increased 1.7-fold (P < 0.001 vs. saline-treated controls). In subsequent in vitro binding studies, formononetin competitively bound murine mammary estrogen receptors, but with a relative binding affinity 15,000 times less potent than that of estradiol-17 beta. The results demonstrate an ability of formononetin to support mammary gland proliferation. However, the estrogenic potency of formononetin appears extremely weak compared with that of estradiol-17 beta and is roughly proportional to estrogen receptor-binding capacity.
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PMID:Proliferative response of mammary glandular tissue to formononetin. 764 82


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