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C Schairer

Publications and source records attributed to C Schairer.

At least 19 recordsLinked to original sources
PubMed2006

Risk of breast, ovary, and uterine corpus cancers among 85,268 women with AIDS.

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 (Ptrend=0.47) or AIDS-relative time (Ptrend=0.14) or after adjustment for established cancer risk factors. However, it increased significantly between 1980 and 2002 (Ptrend=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.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Effects of mammographic density and benign breast disease on breast cancer risk (United States).

BACKGROUND: Having either a history of benign breast disease, particularly atypical hyperplasia or extensive mammographic breast density, is associated with increased breast cancer risk. Previous studies have described an association between benign breast disease histology and breast density. However, whether these features measure the same risk, or are independent risk factors, has not been addressed. METHODS: This case-control study, nested within the prospective follow-up of the Breast Cancer Detection Demonstration Project, evaluated both benign histologic and mammographic density information from 347 women who later developed breast cancer and 410 age- and race-matched controls without breast cancer. Multivariate logistic regression analyses provided maximum-likelihood estimates of the odds ratios (OR) and 95% confidence intervals (CI) to evaluate the relative risk of breast cancer associated with each exposure. RESULTS: Adjusting for mammographic density, the OR for atypical hyperplasia was 2.1 (95% CI: 1.3-3.6), and adjusting for benign breast histology, the OR for > or = 75% density was 3.8 (95% CI: 2.0-7.2). Women with nonproliferative benign breast disease and > or = 75% density had an OR of 5.8 (95% CI: 1.8-18.6), and women with < 50% density and atypical hyperplasia had an OR of 4.1 (95% CI: 2.1-8.0). CONCLUSIONS: In this study, both benign breast disease histology and the percentage of the breast area with mammographic density were associated with breast cancer risk. However, women with both proliferative benign breast disease and > or = 75% density were not at as high a risk of breast cancer due to the combination of effects (p = 0.002) as women with only one of these factors.

Adult↗
PubMed2000

Dietary fat, fat subtypes, and breast cancer in postmenopausal women: a prospective cohort study.

BACKGROUND: The intake of total dietary fat and of certain fat subtypes has been shown to be strongly associated with breast cancer in international comparisons and in animal experiments. However, observational epidemiologic studies have generally reported either weak positive or no associations. To extend the prospective epidemiologic evidence on this question, we examined the association between adult dietary intake of fat, fat subtypes, and breast cancer in a large, prospective cohort of postmenopausal women. METHODS: Participants were selected from a national breast cancer mammography screening program conducted from 1973 through 1981 at 29 centers throughout the United States. From 1987 through 1989, 40022 postmenopausal women satisfactorily completed a mailed, self-administered questionnaire that included a 60-item National Cancer Institute/Block food-frequency questionnaire. Women were then followed for an average of 5.3 years; 996 women developed breast cancer. Risk was assessed by use of Cox proportional hazard regression, with age as the underlying time metric. All statistical tests were two-sided. RESULTS: Compared with women in the lowest quintile (Q1) of percentage of energy from total fat, the adjusted risk ratio (RR) and 95% confidence interval (CI) for women in the highest quintile (Q5) was 1.07 (95% CI = 0.86-1.32). In analyses stratified by history of benign breast disease (BBD), a positive association was observed among only women with no history of BBD (RR (Q5 versus Q1) = 2.20; 95% CI = 1.41-3.42; test for trend, P =.0003). The increased risk in these women appeared to be attributable to unsaturated fat intake and oleic acid in particular. CONCLUSIONS: In this study, there was no overall association between fat intake during adulthood and breast cancer risk; however, among women with no history of BBD, there appeared to be a positive association between total and unsaturated fat intake and breast cancer risk.

Breast Neoplasms↗
PubMed2000

A prospective study of diet quality and mortality in women.

CONTEXT: Most studies of diet and health care have focused on the role of single nutrients, foods, or food groups in disease prevention or promotion. Few studies have addressed the health effects of dietary patterns, which include complex mixtures of foods containing multiple nutrients and nonnutrients. OBJECTIVE: To examine the association of mortality with a multifactorial diet quality index. DESIGN AND SETTING: Data from phase 2 (1987-1989) of a prospective cohort study of breast cancer screening, the Breast Cancer Detection Demonstration Project, with a median follow-up of 5.6 years. PARTICIPANTS: A total of 42,254 women (mean age, 61.1 years) who completed the food frequency questionnaire portion of the survey. MAIN OUTCOME MEASURE: All-cause mortality by quartile of Recommended Food Score (RFS; the sum of the number of foods recommended by current dietary guidelines [fruits, vegetables, whole grains, low-fat dairy, and lean meats and poultry] that were reported on the questionnaire to be consumed at least once a week, for a maximum score of 23). RESULTS: There were 2065 deaths due to all causes in the cohort. The RFS was inversely associated with all-cause mortality. Compared with those in the lowest quartile, subjects in the upper quartiles of the RFS had relative risks for all-cause mortality of 0.82 (95% confidence interval [CI], 0.73-0.92) for quartile 2, 0.71 (95% CI, 0.62-0.81) for quartile 3, and 0.69 (95% CI, 0.61-0.78) for quartile 4 adjusted for education, ethnicity, age, body mass index, smoking status, alcohol use, level of physical activity, menopausal hormone use, and history of disease (chi2 for trend = 35.64, P<.001 for trend). CONCLUSIONS: These data suggest that a dietary pattern characterized by consumption of foods recommended in current dietary guidelines is associated with decreased risk of mortality in women.

Adult↗
PubMed2000

Menopausal estrogen and estrogen-progestin replacement therapy and breast cancer risk.

CONTEXT: Whether menopausal hormone replacement therapy using a combined estrogen-progestin regimen increases risk of breast cancer beyond that associated with estrogen alone is unknown. OBJECTIVE: To determine whether increases in risk associated with the estrogen-progestin regimen are greater than those associated with estrogen alone. DESIGN: Cohort study of follow-up data for 1980-1995 from the Breast Cancer Detection Demonstration Project, a nationwide breast cancer screening program. SETTING: Twenty-nine screening centers throughout the United States. PARTICIPANTS: A total of 46355 postmenopausal women (mean age at start of follow-up, 58 years). MAIN OUTCOME MEASURE: Incident breast cancers by recency, duration, and type of hormone use. RESULTS: During follow-up, 2082 cases of breast cancer were identified. Increases in risk with estrogen only and estrogen-progestin only were restricted to use within the previous 4 years (relative risk [RR], 1.2 [95% confidence interval [CI], 1.0-1.4] and 1.4 [95% CI, 1.1-1.8], respectively); the relative risk increased by 0.01 (95% CI, 0.002-0.03) with each year of estrogen-only use and by 0.08 (95% CI, 0.02-0.16) with each year of estrogen-progestin-only use among recent users, after adjustment for mammographic screening, age at menopause, body mass index (BMI), education, and age. The P value associated with the test of homogeneity of these estimates was .02. Among women with a BMI of 24.4 kg/m2 or less, increases in RR with each year of estrogen-only use and estrogen-progestin-only use among recent users were 0.03 (95% CI, 0.01-0.06) and 0.12 (95% CI, 0.02-0.25), respectively. These associations were evident for the majority of invasive tumors with ductal histology and regardless of extent of invasive disease. Risk in heavier women did not increase with use of estrogen only or estrogen-progestin only. CONCLUSION: Our data suggest that the estrogen-progestin regimen increases breast cancer risk beyond that associated with estrogen alone.

Body Mass Index↗
PubMed2000

Risk of myocardial infarction after oophorectomy and hysterectomy.

To determine the risk of developing a first myocardial infarction after a hysterectomy and/or oophorectomy. Case-cohort analysis performed among 17,126 women in the Uppsala Health Care Region of Sweden, who had undergone a hysterectomy and/or oophorectomy in 1965 to 1983. Record linkage was used for follow-up and medical records to ascertain the actual history of oophorectomy. Risk estimates were calculated by relating the observed number of cases in the cohort to that expected on the basis of incidence rates in the population. Overall, 214 cases of myocardial infarction were observed. In premenopausal women a bilateral oophorectomy alone tended to increase the relative risk 1.6; 95% CI 0.8-3.1, but this operation combined with hysterectomy increased the risk only among those aged 50 and over at surgery. Hysterectomy at premenopausal age or unilateral oophorectomy did not alter the risk of myocardial infarction. In naturally menopausal women, hysterectomy-mainly for uterine myoma-was associated with a four-fold increase in relative risk (3.8; 95% CI 1.9-7.8). Hysterectomy for treatment of myoma performed after a natural menopause is linked to an excess risk for myocardial infarction. Bilateral oophorectomy before menopause may increase the risk of myocardial infarction.

Adult↗
PubMed2000

Comparison of industrial hygienists' exposure evaluations for an epidemiologic study.

OBJECTIVES: A study was conducted to determine what level of information is required by industrial hygienists before they can develop exposure estimates comparable with those developed from a more in-depth evaluation. METHODS: Three industrial hygienists evaluated formaldehyde exposures of 300 jobs selected from an earlier epidemiologic study. The jobs were evaluated over the following 6 cycles: (i) job title and industry; (ii) job title, industry, dates; (iii) job and department title and industry; (iv) cycle 3 information with dates; (v) cycle 3 information with a plant report; and (vi) job and department title, industry, dates, and the report. Each hygienist assigned jobs to 1 of 4 exposure categories, which were compared with the categories in the original epidemiologic study. RESULTS: Overall, the mean differences between the hygienists' evaluations and the standard, although small, changed little over the cycles. The kappa statistic was poor to moderate for all the cycles, but the agreement was greater than expected due to chance. There was moderate improvement in overall agreement over the cycles using the weighted kappa statistic, but little improvement in the intraclass correlation coefficients of the hygienists' evaluations, which ranged from 0.4 to 0.5. Department information improved the agreement with the standard by 5--10%, but dates did not the improve agreement. There were some differences by type of plant, job function, exposure level, and date of the estimate. Using a hypothetical exposure-response scenario, this level of misclassification would have resulted in missing an association. CONCLUSIONS: Although there was slight improvement with increasing levels of information, these findings suggest that the subjective categorical assessment of exposures by industrial hygienists will not produce exposure estimates comparable to more in-depth evaluations of exposure.

Epidemiologic Methods↗
PubMed1999

Estrogen replacement therapy and breast cancer survival in a large screening study.

BACKGROUND: Hormone replacement therapy has been associated in some studies with reductions in breast cancer mortality among women who develop this disease. It is unclear whether this association reflects the biologic activity of the hormones or the earlier detection of tumors among hormone users. We examined breast cancer mortality among women who were diagnosed with axillary lymph node-negative and node-positive breast cancer according to the currency of estrogen use at diagnosis. METHODS: Vital status through June 1995 was determined for 2614 patients with postmenopausal breast cancer diagnosed during the period from 1973 to January 1981. We estimated adjusted hazard-rate ratios (adjusting for tumor size, age, race, Quetelet [body mass] index, and number of positive lymph nodes in women with node-positive disease) and unadjusted cumulative probabilities of breast cancer death over time since diagnosis. RESULTS: Among patients with node-negative disease, rate ratios for breast cancer mortality associated with current use compared with nonuse at diagnosis were 0.5 (95% confidence interval [CI] = 0.3-0.8) until 144 months after diagnosis and 2.2 (95% CI = 0.9-5.2) thereafter. Mortality was not statistically significantly lower in past users. The cumulative probabilities of breast cancer mortality at the end of follow-up were 0.14, 0.14, and 0.09 in nonusers, past users, and current users, respectively. Among women with node-positive disease, the rate ratios associated with current and past use were both 0.5 until 48 months after diagnosis (95% CI = 0.3-0.8 for current users; 95% CI = 0.3-0.9 for past users) and were 1.1 (95% CI = 0.7-1.7) and 1.8 (95% CI = 1.2-2.7), respectively, thereafter. The cumulative probabilities of breast cancer mortality were 0.32, 0.39, and 0.27 in nonusers, past users, and current users, respectively. CONCLUSIONS: Patients with breast cancer who were using replacement estrogens at the time of diagnosis experienced reductions in breast cancer mortality, which waned with the time since diagnosis.

Aged↗
PubMed1999

Risks of breast and endometrial cancer after estrogen and estrogen-progestin replacement.

OBJECTIVE: We studied the risk of breast and endometrial cancer in a cohort of 11,231 Swedish women prescribed different replacement hormone regimens. METHODS: All 10,472 women at risk of developing breast cancer and 8,438 women at risk of endometrial cancer were followed up from the time of the questionnaire in 1987-88 through 1993, by record-linkages to the National Swedish Cancer Registry. Using data from a questionnaire we analyzed the relationships between hormone exposures and cancer risk, with non-compliers and users of less than 1 year as a reference group. RESULTS: For breast cancer, women reporting use of estrogens combined with progestins had evidence of an increased risk relative to women denying intake or taking hormones for less than 1 year; relative risk (RR) = 1.4 (95% confidence interval 0.9-2.3) after 1-6 years of intake, and RR = 1.7 (95% CI 1.1-2.6) after more than 6 years. This excess risk seemed confined to recent exposure. We found no association with intake of estrogens alone using non-compliers and short-term takers as the reference group. The risk of invasive endometrial cancer was increased four-fold in women using medium-potency estrogens alone for 6 years or longer, RR = 4.2 (95% CI 2.5-8.4). Women on such long-term progestin-combined treatment had a lower, non-significant, excess risk (RR = 1.4; 95% CI 0.6-3.3). CONCLUSIONS: We conclude that long-term recent use of estrogen-progestin combined replacement therapy may increase the risk of breast cancer. Exposure to estrogen alone substantially elevates the risk of endometrial cancer, an increase that can be reduced or perhaps avoided by adding progestins.

Breast Neoplasms↗
PubMed1997

Breast cancer risk associated with gynecologic surgery and indications for such surgery.

Risk of breast cancer was assessed in relationship to gynecologic operations using data from a record-linkage study involving 15,844 women in the Uppsala Health Care Region of Sweden, who underwent surgery between 1965 and 1983. Data abstracted from medical records for the breast cancer cases and a random sample of the cohort allowed examination of risk associated with these operations in regard to menopausal status and indications for the operations. Among women who were pre-menopausal at the time of operation, a bilateral oophorectomy before the age of 50 years was associated with a 50% reduction in the risk of breast cancer compared with the background population, a reduction in risk evident within 10 years of the operation. A bilateral oophorectomy after the age of 50 years in pre-menopausal women or after a natural menopause was not associated with any reduction in risk. There were no reductions in risk associated with a unilateral oophorectomy or hysterectomy among women who were pre-menopausal at the time of operation. In fact, hysterectomy alone was associated with a slight increase in breast cancer risk when the operation was due to myomas, abnormal bleeding, and, possibly, severe forms of endometriosis but not to other reasons. Risk did not vary substantially by indications for oophorectomy, including benign ovarian neoplasms and functional ovarian cysts, though endometriosis was associated with a non-significant increase in breast cancer risk.

Adult↗
PubMed1997

A prospective study of menopausal hormones and risk of colorectal cancer (United States)

The relation of colorectal cancer and its subsites with use of menopausal hormones was evaluated in the United States among 40,464 postmenopausal women, 41 to 80 years of age, who initially volunteered for a nationwide breast-cancer screening program and were followed for an average of 7.7 years. Ever-use of menopausal hormones was not associated with risk of total colorectal cancers (relative risk [RR] = 0.99, 95 percent confidence interval [CI] = 0.79-1.2) or cancers of the colon (RR = 1.1, CI = 0.81-1.6) or rectum (RR = 1.1, CI = 0.59-1.9). Recent hormone users, however, had a small nonsignificant reduction in risk of colorectal cancer (RR = 0.78, CI = 0.55-1.1), which was most pronounced for distal colon (RR = 0.68, CI = 0.29-1.6) and rectal tumors (RR = 0.64, CI = 0.24-1.7). No effect was observed for former hormone users, and risk generally did not vary by time since last use, type of regimen, or duration of use. However, the reduced risk for recent users was stronger for users of five or more years' duration. These data show some lowering of colorectal cancer risk among recent menopausal hormone users of long duration.

Adult↗
PubMed1997

Cause-specific mortality in women receiving hormone replacement therapy.

To assess the risks and benefits of menopausal hormone replacement therapy, we followed a 23,346-member, population-based cohort of Swedish women who were prescribed menopausal estrogens for an average of 8.6 years for mortality. Compared with the general population, the standardized mortality ratio for all-cause mortality in this cohort was 0.77 (95% confidence limits = 0.73, 0.81). Deaths in each of the 12 major categories of causes of death except for injuries occurred 12% to 86% less frequently than expected. We examined in detail four specific causes of death according to the type of hormone prescribed, namely weak estrogens (primarily estriol), more potent estrogens (primarily estradiol and conjugated estrogens) in combination with a progestin, and more potent estrogens without a progestin. Mortality from endometrial cancer was not related to the prescription of weak estrogens or an estrogen-progestin combination, but mortality was 40% higher in women prescribed more potent estrogens without a progestin. Women prescribed weak estrogens, more potent estrogens, and the combined estrogen-progestin regimen were at reduced risk of death from ischemic heart disease (standardized mortality ratios of 0.7, 0.6, and 0.4, respectively). The more potent estrogens and the estrogen-progestin combination were associated with a marked reduction in risk of intracerebral hemorrhage (standardize mortality ratios of 0.4 and 0.6, respectively) and "other" cerebrovascular disease, but not other types of stroke. The concern that use of progestins would lead to psychic disorders related to suicide received no support from our results. Breast cancer results are described elsewhere. These data provide little evidence of an adverse effect of the combined estrogen-progestin regimen as compared with estrogens alone on mortality. They do indicate, however, that both selection factors and biology may contribute to the almost across-the-board-reduction in mortality associated with hormone replacement therapy.

Adult↗
PubMed1997

Reproductive factors, oral contraceptive use, and risk of colorectal cancer.

Multiparity and use of oral contraceptives are hypothesized to reduce risk of colorectal cancer. Among 57,529 women, 31-90 years of age, who volunteered for a nationwide breast cancer screening program from 1973 to 1980, we observed 154 pathologically confirmed cases of colon cancer and 49 cases of rectal cancer in up to 10 years of follow-up (388,555 person-years). Parity was not associated with risk of colorectal cancer [age-adjusted rate ratio for > or = 4 children vs no children = 1.0; 95% confidence interval (CI) = 0.72-1.5], although decreases in proximal colon cancer and increases in distal colon cancer were observed among parous women. The effect of parity did not vary by age at diagnosis. We found no strong or consistent association for age at menarche, age at first birth, or age at natural menopause. In addition, oral contraceptive use, reflecting mainly past use, was unrelated to risk of colorectal cancer (rate ratio = 1.0; 95% CI = 0.75-1.4). These findings do not corroborate the hypothesis that reproductive events or oral contraceptives influence the development of colorectal cancer.

Adult↗
PubMed1996

Cancer incidence and mortality in women receiving estrogen and estrogen-progestin replacement therapy--long-term follow-up of a Swedish cohort.

We analyzed cancer incidence and mortality in a cohort of 22,597 Swedish women who were prescribed replacement hormones. After 13 years of follow-up in national registries, 2,330 incident cancer cases and 848 cancer deaths were observed. Overall, our results were reassuring since incidence rate ratios (SIRs) for 16 cancer sites and mortality ratios (SMRs) for all 10 examined sites were at, or lower than, unity. However, we found that exposure to an estrogen-progestin combined brand was associated with an increasing relative risk of breast cancer with follow-up time, the SIR reaching 1.4 (95% CI 1.1-1.8) after 10 years of follow-up. The relative risk of endometrial cancer was substantially increased, with the highest SIR of 5.0 (95% CI 1.6-5.9) in women prescribed estrogens alone, whereas those given an estrogen-progestin combination showed no elevation in risk. The risk estimates for liver and biliary tract cancers and for colon cancer were reduced by about 40%, notably in women prescribed the estradiol-progestin compound. Further detailed analyses revealed no evidence of adverse or protective effects on the risk of ovarian, uterine cervical, vulvar/vaginal, rectal, pancreatic, renal, lung, thyroid and other endocrine cancers, brain tumors, malignant melanoma or other skin cancers. Hormone replacement therapy was not associated with an increase in mortality for any cancer site, at this time of follow-up. For breast and endometrial cancers, SMRs were below baseline but tended to increase with follow-up time. We conclude that hormone replacement increases the endometrial-cancer risk after unopposed estrogens and the breast-cancer risk-notably after estrogen-progestin combined therapy-and tentatively suggest that it exerts a protective effect against colon and liver cancer risks.

Aged↗
PubMed1996

Prospective study of relative weight and risk of breast cancer: the Breast Cancer Detection Demonstration Project follow-up study, 1979 to 1987-1989.

Despite extensive research on obesity and breast cancer in recent decades, inconsistencies in the literature exist. The authors examined prospectively the relation between adult relative weight (weight (kg)/height (m)1.5) and breast cancer risk in a cohort of 54,896 women aged 31-89 years who had previously participated in the Breast Cancer Detection Demonstration Project. During a mean follow-up period of 7 years, 226 of the premenopausal women and 1,198 of the postmenopausal women developed breast cancer. Analysis was performed using Cox proportional hazards regression methods with age as the underlying time variable and adjusted for the effects of potential confounders. Among postmenopausal women, the risk of breast cancer increased with increasing relative weight (p < 0.05 for trend); relative risk for the highest compared with the lowest quintile for relative weight was 1.3 (95% confidence interval (CI) 1.1-1.6). This association was modified by age at diagnosis, with relative risks of 1.1 (95% CI 0.8-1.4), 1.2 (95% CI 0.8-1.7), and 1.8 (95% CI 1.3-2.5), respectively, for women aged < 60, 60-64, and > or = 65 years. The higher risk of breast cancer among the older and overweight women was largely confined to women whose weights were measured during the postmenopausal but not the premenopausal period. This risk pattern was observed among the naturally menopausal women, but was also apparent in the smaller group of women with bilateral oophorectomy or hysterectomy with one ovary retained. Among premenopausal women, adult relative weight was not associated with breast cancer risk. These findings suggest that the inconsistencies in the literature on obesity and breast cancer may be due in part to the differing age distributions of the populations studied. The authors conclude that prevention of obesity throughout adulthood, particularly after menopause, may help reduce breast cancer among older women.

Adult↗