Search

Steroid 5-alpha-reductase type 2 (SRD5a2) is a critical enzyme in androgen metabolism. Two polymorphisms in the SRD5a2 gene, V89L (rs523349) and A49T (rs9282858), have been studied for associations with prostate cancer risk, with conflicting results. The authors conducted a systematic review and meta-analysis (1997-2007) to examine these associations and compared the results with findings from genome-wide association studies of prostate cancer. The meta-analysis included 24 case-control studies (10,088 cases and 10,120 controls for V89L and 4,998 cases and 5,451 controls for A49T). The authors found that prostate cancer was not associated with V89L (L allele vs. V allele: odds ratio = 0.99, 95% confidence interval: 0.94, 1.05) and was probably not associated with A49T (T allele vs. A allele: odds ratio = 1.10, 95% confidence interval: 0.86, 1.40). These results could have been distorted by spectrum-of-disease bias, convenience sampling of cases and controls, genotype misclassification, and/or confounding. Neither V89L nor A49T was included in microarray chips used for published genome-wide association studies. Analysis of well-designed population-based studies with pathway-based arrays containing common genetic variants could be useful for identifying genetic factors in prostate cancer. [ABSTRACT FROM AUTHOR]

This randomized clinical trial examined the feasibility of low-fat dietary interventions among postmenopausal women of diverse backgrounds. During 1992-1994, 2,208 women aged 50-79 years, 28% of whom were black and 16% Hispanic, enrolled at clinics in Atlanta, Georgia, Birmingham, Alabama, and Miami, Florida. Intervention/support groups met periodically with a nutritionist to reduce fat intake to 20% of energy and to make other diet modifications. At 6 months postrandomization, the intervention group reduced fat intake from 39.7% of energy at baseline to 26.4%, a reduction of 13.3% of energy, compared with 2.3% among controls. Saturated fatty acid and cholesterol intakes were reduced, but intakes of fruits and vegetables, but not grain products, increased. Similar effects were observed at 12 and 18 months. Black and non-Hispanic white women had similar levels of reduction in fat, but the decrease in Hispanic women was less. Changes did not vary significantly by education. While bias in self-reported intakes may have resulted in somewhat overestimated changes in fat intake, the reported reduction was similar to the approximately 10% of energy decrease found in most trials and suggests that large changes in fat consumption can be attained in diverse study populations and in many subgroups. [ABSTRACT FROM AUTHOR]

This report describes the associations of race/ethnicity and years of education with the validity, reliability, and bias of a self-administered food frequency questionnaire (FFQ) designed to be sensitive to low-fat, regional, and ethnic dietary patterns. Data were from the Women's Health Trial Feasibility Study in Minority Populations, a randomized clinical trial conducted between 1992 and 1994 to test the feasibility of a low-fat dietary intervention that targeted low-income, black, and Hispanic women. Of 1,015 participants eligible for these analyses, 28.1% were black, 16.2% were Hispanic, and 12.3% had not completed high school. The analyses focused on percentage of energy obtained from fat, and used 4-day food records as the criterion instrument. Validity at baseline, defined as the correlation between FFQs and food records, was lower among blacks than among whites (0.26 vs. 0.49; p < 0.001), did not differ between Hispanics and whites, and was lower among women with fewer years of education (0.19, 0.35, 0.49, and 0.42 for <12, 12, 13-15, and > or =16 years of education, respectively; for trend, p < 0.05). Six months after randomization, validity increased in most race/ethnicity and education subgroups, and differences across groups became small and statistically nonsignificant. Validity increased significantly among participants receiving the dietary intervention, while increases among control women were somewhat smaller. Reliability, defined as the correlation between baseline and 6-month measures among controls, was similar across racial/ethnic and educational groups. Bias at baseline, defined as the mean value from the FFQ minus the mean from the food record, was 4.6 percentage points of energy from fat; it was lowest among blacks (p < 0.01) and did not differ by years of education. These results suggest that special protocols which address participant training may be necessary when using self-administered FFQs in minority or poorly educated populations. [ABSTRACT FROM AUTHOR]

Breast cancer is diagnosed at a younger age and a more advanced stage in African-American women than in White women. The authors investigated the effects of several factors, including race, on stage of breast cancer in women aged 20-54 years living in Atlanta, Georgia, and diagnosed between 1990 and 1992. A total of 251 African-American and 580 White women were interviewed and their medical records reviewed. By use of polytomous logistic regression, factors possibly influencing stage and racial differences in stage were studied. In African-American women, the odds of stage III/IV breast cancer at diagnosis were almost four times the odds in White women (odds ratio = 3.79, 95% confidence interval: 2.45, 5.89) and approximately two and one-half times for stage IIA or stage IIB disease (odds ratio = 2.57, 95% confidence interval: 1.66, 3.99; odds ratio = 1.94, 95% confidence interval: 1.31, 2.86, respectively). These racial differences appeared to be largely explained by insurance status, poverty, history of mammography, method of tumor detection, and obesity. Interventions targeting these factors could potentially lower the stage at diagnosis for African-American breast cancer patients and, in doing so, improve their survival and other outcomes.

As part of a case-control study of the efficacy of screening mammography, the authors validated the mammography histories of 2,495 women aged 40-64 years with incident breast cancer diagnosed in 1994-1998 and a 25% random sample of 615 controls never diagnosed with breast cancer, all reporting a mammogram in the past 5 years. Subjects from five metropolitan areas of the United States were cross-classified by facility records ("gold standard") and self-report according to history of a recent screening mammogram (within 1 year or within 2 years). Sensitivity and specificity of self-reported screening at 1 year were 0.93 and 0.82, respectively, for cases and 0.92 and 0.80 for controls. At 2 years, sensitivity and specificity were 0.97 and 0.78 for both cases and controls. Confidence intervals for the differences in sensitivity and specificity were narrow and included zero. Scant evidence was found of telescoping (recollection of events as more recent than actual). Findings suggest that, in an interview-based case-control study of the efficacy of screening mammography, 1) estimated true prevalences of recent screening mammography adjusted for sensitivity and specificity will be slightly lower than self-reported prevalences, and 2) differential misclassification of exposure status is slight. Therefore, odds ratios will likely be biased toward the null, underestimating screening efficacy.

The Diet Quality Index (DQI) was developed to measure overall dietary patterns and to predict chronic disease risk. This study examined associations between DQI and short-term all-cause, all-circulatory-disease, and all-cancer mortality in the American Cancer Society Cancer Prevention Study II Nutrition Cohort, a cohort of US adults aged 50-79 years enrolled in a prospective study. After 4 years of follow-up (1992-1996), there were 869 deaths among 63,109 women and 1,736 deaths among 52,724 men. All study participants reported being disease free at baseline in 1992-1993. In age-adjusted Cox models, a higher DQI, which was indicative of a poorer quality diet, was positively related to all-cause and all-circulatory-disease mortality rates in both women and men and to cancer mortality in men only. However, in fully adjusted Cox models, only circulatory disease mortality was clearly positively related to DQI and only in women (medium-low-quality diet vs. highest-quality diet: rate ratio = 1.86, 95% confidence interval: 1.19, 2.89). Although trend tests indicated significant positive relations between DQI and all-cause mortality, effects were small (rate ratios

To gain insight into whether breast cancer tumors jointly classified by estrogen receptor (ER) and progesterone receptor (PR) status represent diseases with differing etiologies, data from a population-based case-control study of US women 20-44 years of age were analyzed. Cases included 1,556 women diagnosed between 1990 and 1992. Age- and geographic-frequency-matched controls included 1,397 women identified by random digit dialing. Heterogeneity between ER+PR+ and ER-PR- tumors was most pronounced in relation to age, race, and recreational exercise at 12-13 years of age. Multivariate-adjusted odds ratios for ER+PR+ tumors were 0.64 (95% confidence interval (CI): 0.47, 0.89) for 30-34 versus 40-44 years of age, 0.89 (95% CI: 0.63, 1.25) for Black versus White race, and 0.84 (95% CI: 0.68, 1.03) for exercise at 12-13 years of age above versus at or below the median. Corresponding odds ratios for ER-PR- tumors were 1.24 (95% CI: 0.86, 1.77), 1.51 (95% CI: 1.07, 2.14), and 1.15 (95% CI: 0.90, 1.48). Risk of ER-PR- cancer in relation to menstrual and reproductive (parity and lactation) characteristics, alcohol consumption, and family history of breast cancer was similar to that observed for ER+PR+ tumors. These findings only modestly support the hypothesis that hormonally related risk factors have differing relations with ER+PR+ versus ER-PR- tumors among younger women.

Random digit dialing is used frequently in epidemiologic case-control studies to select population-based controls, even when both cases and controls are interviewed face-to-face. However, concerns persist about the potential biases of random digit dialing, particularly given its generally lower response rates. In an Atlanta, Georgia, case-control study of breast cancer among women aged 20-54 years, all of whom were interviewed face-to-face, two statistically independent control groups were compared: those obtained through random digit dialing (n = 652) and those obtained through area probability sampling (n = 640). The household screening rate was significantly higher for the area sample, by 5.5%. Interview response rates were comparable. The telephone sample estimated a significantly larger percentage (by approximately 7%) of households to have no age-eligible women. Both control groups, appropriately weighted, had characteristics similar to US Census demographic characteristics for Atlanta women, except that respondents in both control groups were more educated and more likely to be married. The authors conclude that households contacted through random digit dialing are somewhat less likely to participate in the household screening process, and if they are cooperative, some households may not disclose that age-eligible women reside therein. Investigators need to develop improved methods for screening and enumerating household members in random digit dialing surveys that target a specific subpopulation, such as women.

To investigate whether use of electric blankets, one of the largest sources of electromagnetic field exposure in the home, is associated with the risk of female breast cancer, the authors analyzed data from a population-based US case-control study. The 2,199 case patients were under age 55 years and had been newly diagnosed with breast cancer between 1990 and 1992. The 2,009 controls were frequency-matched to cases by 5-year age group and geographic area. There was little or no risk associated with ever having used electric blankets, mattress pads, or heated water beds among women under age 45 years (adjusted odds ratio = 1.01, 95% confidence interval 0.86-1.18) or among women aged > or =45 years (adjusted odds ratio = 1.12, 95% confidence interval 0.87-1.43). There was no substantial variation in risk with duration of use; with whether the appliance was used only to warm the bed or used throughout the night; with menopausal status; or with the cases' hormone receptor status or stage of disease. Potential breast cancer risk factors that were associated with electric blanket use did not substantially confound the associations under investigation. These data do not support the hypothesis that electric blanket use increases breast cancer risk among women under age 55 years.

To evaluate whether recreational physical activity is associated with breast cancer among young women, the authors analyzed data from a population-based case-control study. Cases (n = 1,668) were women under age 45 years who had been newly diagnosed with breast cancer between 1990 and 1992 in Atlanta, Georgia, central New Jersey, or Seattle, Washington. Controls (n = 1,505) were frequency-matched to cases by 5-year age group and geographic area of residence. Breast cancer was not associated with recreational activity in any of the three time periods assessed (highest quartile of activity vs. lowest: age- and center-adjusted odds ratio (OR) = 0.94 (95% confidence interval (CI) 0.77-1.15) at ages 12-13 years, OR = 1.08 (95% CI 0.88-1.32) at age 20 years, and OR = 1.18 (95% CI 0.97-1.44) during the past year), with the average of the three time periods (OR = 1.02, 95% CI 0.84-1.25), or with daily climbing of at least two flights of stairs (without stopping) during the past year (daily climbing vs. never climbing: OR = 1.03, 95% CI 0.86-1.23). Estimates were not modified or confounded by body mass index, menopausal status, or caloric intake during the past year. These results do not support a protective role for physical activity in the risk of breast cancer among young women.

Some studies (but not all) have suggested that there may be an increase in the risk of breast cancer associated with a prior induced abortion. The risk, if present, may vary according to the duration of the pregnancy in which the abortion occurred, or to a woman's age or parity at that time. The authors conducted a case-control study of breast cancer in white women under age 45 years to address the question of breast cancer risk in relation to induced abortion, with the intention of identifying subgroups of women who might be at particularly increased risk. White women who were diagnosed with breast cancer (n = 1,302) from May 1, 1990, through December 31, 1992, in three geographic regions of the United States (Atlanta, Georgia; Seattle/Puget Sound, Washington; and five counties in central New Jersey) were interviewed about their reproductive histories, including the occurrence of induced abortion. Similar information was obtained from control women identified through random digit dialing. Logistic regression analysis was used to estimate the relative risk of breast cancer associated with a history of induced abortion, controlling for the potentially confounding influence of other breast cancer risk factors. Among women who had been pregnant at least once, the risk of breast cancer in those with a prior induced abortion was 20% higher than that in women with no history of abortion (95% confidence interval 1.0-1.5). This small increase in risk varied little according to number of abortions or a woman's current age. The association was present primarily among nulliparous women whose abortions occurred prior to 9 weeks' gestation (estimated relative risk = 2.0, 95% confidence interval 1.2-3.3). There was no excess risk of breast cancer associated with induced abortion among parous women. These data support the hypothesis that there may be a small increase in the risk of breast cancer related to a history of induced abortion among young women of reproductive age. However, the data from this study and others do not permit a causal interpretation at this time; neither do the collective results of the studies suggest that there is a subgroup of women in whom the relative risk associated with induced abortion is unusually high.

In a multicenter population-based case-control study that included 1,588 cases and 1,394 controls less than age 45 years, the authors examined the relation of adult body size and breast cancer risk among young women. Breast cancer patients and healthy controls were identified in Atlanta, Georgia; Seattle/Puget Sound, Washington; and central New Jersey. Cases were newly diagnosed with in situ or invasive breast cancer during the period of May 1, 1990, through December 31, 1992. Anthropometric variables thought to reflect early environmental factors (e.g., height, sitting height, frame size), obesity, and body fat distribution were measured directly. Height, but not sitting height or frame size, was a breast cancer risk factor. Risk of the disease was increased 46 percent among women in the fourth quartile of height (> 167 cm) compared with women in the first quartile (< 159 cm). Body weight, but not body fat distribution, was related to breast cancer risk. Risk of the disease was 35 percent lower among women in the highest quartile of Quetelet index (> 28.8 kg/m2) compared with women in the lowest quartile (< 22.0 kg/m2). Risk of the disease was increased about 2.1-fold (95 percent confidence interval 1.2-3.8) among women who were thin and tall compared with women who were heavy and short. Thus, breast cancer risk was increased substantially among younger women with a linear body type.

Survival differences have been noted between black women and white women with breast cancer. It is hypothesized that a prolonged interval between initial medical consultation and establishment of a diagnosis (system delay), resulting in a more advanced stage of disease at diagnosis, might explain part of this survival difference. This study was performed to determine whether system delay differs between black and white breast cancer patients, and to examine predictors of delay in blacks and whites. The study population consisted of 996 female breast cancer patients from the National Cancer Institute's Black/White Cancer Survival Study, a cohort study carried out in 1985-1986 in the metropolitan areas of Atlanta, Georgia, New Orleans, Louisiana, and San Francisco/Oakland, California. The median system delay was slightly longer for blacks than for whites--2.7 weeks versus 2.1 weeks--but this difference was not statistically significant. Having a palpable lump at diagnosis was associated with reduced system delay in both races, while use of a public clinic increased system delay for blacks. Older women were less likely to be subject to longer system delay than younger women, and this effect was somewhat more pronounced in whites. Survival differences between blacks and whites are probably not due to differences in system delay. However, many women had delays of at least 3 months. Given that younger age and the absence of a palpable lump were the factors most predictive of significant system delay, interventions should be targeted specifically toward reducing system delay in younger women who present without the classical painless lump.

The authors examined the relation between use of estrogen replacement therapy and ovarian cancer mortality in a large prospective mortality study of 240,073 peri- and postmenopausal women, none of whom had a prior history of cancer, hysterectomy, or ovarian surgery at enrollment in 1982. During 7 years of follow-up, 436 deaths from ovarian cancer occurred. Cox proportional hazard regression was used to adjust for other risk factors. Ever use of estrogen replacement therapy was associated with a rate ratio for fatal ovarian cancer of 1.15 (95% confidence interval (CI) 0.94-1.42). The mortality rate ratio increased with duration of use prior to entry to this study to 1.40 (95 CI% 0.92-2.11) with 6-10 years of use and 1.71 (95% CI 1.06-2.77) with > or = 11 years of use. The increase in mortality associated with > or = 6 years of use was observed in both current users (rate ratio (RR) = 1.72, 95% CI 1.01-2.90) and former users at study entry (RR = 1.48, 95% CI 0.99-2.22), relative to never users. Risk associated with use was not modified by any of the other risk factors. These data suggest that long-term use of estrogen replacement therapy may increase the risk of fatal ovarian cancer.

Glutathione, a tripeptide found in a variety of foods, may function as an anticarcinogen by acting as an antioxidant and by binding with cellular mutagens. The association between dietary glutathione intake and risk of oral and pharyngeal cancer was investigated using data from 1,830 white participants (855 cases and 975 controls) in a population-based case-control study conducted in New Jersey; metropolitan Atlanta, Georgia; Los Angeles County, California; and Santa Clara and San Mateo counties, south of San Francisco-Oakland, California, during 1984-1985. The estimated relative risk of cancer among people with the highest quartile of glutathione intake from all sources was 0.5 (95% confidence interval 0.3-0.7). When analyzed by dietary source, however, glutathione intakes derived from all vegetables and from meat were not related to risk of cancer. Only glutathione derived from fruit and from vegetables commonly consumed raw was associated with reduced oral cancer risk. Relative to the lowest level of combined intake of fruit and of fruit-derived glutathione, risk of cancer decreased slightly with increasing intake of fruit glutathione. This analysis was limited, however, by the small numbers of subjects with extreme combinations of intakes. Further studies are needed to distinguish the potential effect of glutathione from that of fruit and raw vegetables per se or from the influence of other constituents in these foods.

The National Cancer Institute diet questionnaire was evaluated for use in a low-income black population. Data were collected from 91 women aged 30-69 years who were hospital outpatients in Atlanta, Georgia, June through August, 1988. Six ethnic and regional foods added to the questionnaire were found to be important contributors to intakes of several nutrients. Although 17 records were identified as containing probable recording or reporting errors, intakes of carotenes, alpha-carotene, beta-carotene, cryptoxanthin, and vitamin E were significantly and positively associated with serum levels of their referent nutrients. Among nonsmokers, correlation coefficients ranged from 0.32 to 0.45, adjusted for age, body mass index, alcohol and calorie intakes, medications and vitamin supplement use, and serum cholesterol and triglycerides. When questionnaires containing identified errors were omitted, correlations ranged from 0.30 to 0.54. There were no correlations between dietary intakes of lycopene and lutein and blood levels (-0.06 to 0.09). Among smokers, diet-serum correlations were reduced (0.00 to 0.32). These correlations are similar to those reported in research on vitamin E and carotenoids in other populations. These results suggest that the questionnaire is as valid for use in this population as it is in other populations.

A nested case-control study was conducted to assess the relation between serum levels of selenium and retinol and the subsequent risk of cancer. During the years 1972-1984, in northwest Washington State, 156 cases of cancer were identified among members of two employee cohorts from whom specimens had been previously obtained and stored. Two hundred eighty-seven controls were selected from these cohorts and matched to cases on the basis of employer, age, sex, race, and date of blood draw. Selenium and retinol levels were measured by neutron activation and high pressure liquid chromatography, respectively. Information on known cancer risk factors was collected by telephone interviews of subjects and next of kin. Levels of selenium and retinol were unassociated with the incidence of cancer of all sites combined, both overall and within subgroups defined by age, sex, levels of the other micronutrient, time between blood draw and diagnosis, smoking status, and family history of cancer. These findings suggest that neither serum levels of selenium nor those of retinol have an appreciable effect on the risk of cancer.