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Leslie Bernstein

Publications and source records attributed to Leslie Bernstein.

At least 55 records · Page 3Linked to original sources

Racial differences in the familial aggregation of breast cancer and other female cancers.

Although breast cancer familial aggregation has been studied in Caucasians, information for African-Americans is scant. We used family cancer history from the Women's Contraceptive and Reproductive Experiences study to assess the aggregation of breast and gynecological cancers in African-American and Caucasian families. Information was available on 41,825 first and second-degree relatives of Caucasian and 28,956 relatives of African-American participants. We used a cohort approach in which the relative's cancer status was the outcome in unconditional logistic regression and adjusted for correlated data using generalized estimating equations. Race-specific models included a family history indicator, the relative's age, and type. Relative risk (RR) estimates for breast cancer were highest for first-degree relatives, and the overall RR for breast cancer among case relatives was 1.96 (95% CI = 1.68-2.30) for Caucasian and 1.78 (95% CI = 1.41-2.25) for African-Americans. The effect of CARE participants' reference age on their relatives' breast cancer risk was greatest among first-degree relatives of African-American patients with RRs (95% CI) for ages <45 and > or =45 of 2.97 (1.86-4.74) and 1.48 (1.14-1.92), respectively. Among Caucasians, first-degree relatives of case subjects were at greater risk for ovarian cancer, particularly relatives younger than 45 years (RR (95% CI) = 2.06 (1.02-4.12)), whereas African-American first-degree relatives of case subjects were at increased cervical cancer risk (RR (95% CI) = 2.17 (1.22-3.85). In conclusion, these racially distinct aggregation patterns may reflect different modes of inheritance and/or environmental factors that impact cancer risk.

Adult↗

Anthropometrics, physical activity, related medical conditions, and the risk of non-hodgkin lymphoma.

BACKGROUND: Recent reports suggest that obesity, or conditions associated with obesity, might be risk factors for non-Hodgkin lymphoma (NHL), a cancer with dramatically increasing incidence in western countries over the last several decades. Physical inactivity increases the risk of obesity and of type 2 diabetes, but there are few data on the association of physical activity with risk of NHL. METHODS: We evaluated these factors in a population-based case-control study conducted in Detroit, Iowa, Los Angeles, and Seattle from 1998 to 2000. Incident HIV-negative NHL cases aged 20-74 years were rapidly reported in each area (n = 1321). Controls were identified through random digit dialing and Medicare files, and were frequency matched to cases on sex, age, race, and study site (n = 1057). Risk factor data were collected by in-person interviews and self-administered questionnaires. Unconditional logistic regression was used to estimate the odds ratio (OR) and 95% confidence intervals (CI), adjusted for age, sex, race and study center. RESULTS: High body mass index (OR = 1.73 for 35+ versus <25 kg/m2; 95% CI 1.15-2.59) and history of gallstones (OR = 1.95, 95% CI 1.11-3.40) were positively associated with diffuse NHL, but were not associated with follicular or all NHL combined. Height was positively associated with risk of all NHL combined (OR = 1.38 for >70 versus <65 inches; 95% CI 0.98-1.94), and positive associations were apparent for both diffuse and follicular NHL. Non-occupational physical activity was inversely associated with risk of all NHL combined (ORs with increasing level: 1, 0.75, 0.71, 0.55, 0.68; p-trend = 0.04) and for diffuse and follicular NHL. We observed no association of total energy intake, type 2 diabetes, or hypertension with risk of NHL. In a multivariable model to predict risk of diffuse NHL, BMI (OR = 2.15 for 35+ versus <25 kg/m2; 95% CI 1.09-4.25) and height (OR = 1.63 for 71+ versus <65 inches; 95% CI 0.75-3.57) were positively associated with risk while physical activity was weakly and inversely associated risk (ORs with increasing level: 1, 0.76, 0.72, 0.78, 0.82; p-trend = 0.9). CONCLUSION: BMI and history of gallstones were positively associated with risk of diffuse NHL, supporting a role for obesity in this NHL subtype. Height was positively associated with NHL risk across subtypes, and suggests a role for early life nutrition in NHL risk. Non-occupational physical activity was only weakly and inversely associated with NHL risk after adjustment for obesity, height and alcohol use.

Adult↗

Etiologic clues from the similarity of histology-specific trends in esophageal and lung cancers.

OBJECTIVE: We tested whether descriptive evidence exists for differing roles of specific tobacco constituents on different histologic subtypes of esophageal cancer. Esophageal adenocarcinoma incidence rates are increasing while squamous cell esophageal cancer rates are declining in Westernized countries as are the histology-specific lung counterparts. Squamous cell lung cancers, while caused by smoking, are believed to be caused by different constituents of tobacco smoke than lung adenocarcinomas. Smoking is also a risk factor for esophageal cancers. METHODS: We compared patterns of incidence of squamous cell cancers of the lung with those of squamous cell esophageal cancers, and incidence trends in lung adenocarcinomas with those of esophageal adenocarcinomas during the time period from 1976 to 2000 using data from the population-based Los Angeles Cancer Surveillance Program. RESULTS: Rates of squamous cell esophageal cancer declined in a similar fashion to those of squamous cell lung cancer, while esophageal adenocarcinoma incidence increased at a rate similar to that of lung adenocarcinoma, in both men and women, and blacks and whites. Histology-specific socio-economic gradients in lung and esophageal cancers were also strikingly similar. Increases in esophageal adenocarcinoma were confined to the lower third of the esophagus. CONCLUSIONS: While increases in obesity over time might explain these trends, they are also consistent with a specific effect of some constituent of tobacco smoke working through reflux disease to cause esophageal adenocarcinoma.

Adenocarcinoma↗

Influence of exercise activity on quality of life in long-term breast cancer survivors.

BACKGROUND: Behavioral and lifestyle factors may influence quality of life (QOL) outcomes in breast cancer survivors. METHODS: Information on QOL (Short Form-36, SF-36), lifestyle and survivorship was collected during telephone interviews with 374 breast cancer patients, diagnosed between 1983 and 1988 at ages 40 years or younger and interviewed, on average 13.2 years following diagnosis. These women previously participated in a case-control study soon after their diagnoses, providing information on breast cancer risk factors including exercise activity. We examined the impact of changes in exercise activity (comparing pre- to post-diagnosis levels) on the SF-36 mental and physical health summary scales using regression analyses. RESULTS: A positive change in exercise activity was associated with a higher score on the SF-36 physical health summary scale at follow-up (p = 0.005). Change in exercise activity was not associated with the SF-36 mental health summary scale score. Patients who increased their activity levels did not differ from those who did not in terms of medical or demographic characteristics. CONCLUSION: This study provides one of the longest follow-up periods of breast cancer survivors to date among studies that focus on QOL and is unique in its focus on women diagnosed at a young age. Our results confirm high levels of functioning and well-being among long-term survivors and indicate that women whose exercise activity increased following diagnosis score higher on the SF-36 physical health summary scale. These findings suggest a potential role for exercise activity in maintaining well-being after a cancer diagnosis.

Adult↗

Residential mobility in the California Teachers Study: implications for geographic differences in disease rates.

BACKGROUND: Especially for cancers with long latency periods, such as breast cancer, the issue of residential mobility hinders ecologic analyses seeking to examine the role of environmental contaminants in chronic disease etiology. This study describes and evaluates characteristics associated with residential mobility in a sub-sample of the California Teachers Study (CTS) cohort. METHODS: In 2000, lifetime residential histories were collected for a sub-sample of 328 women enrolled in the CTS; women's degree of residential mobility and associated factors were analyzed. RESULTS: While most women moved many times during their lives (average = 8.9), the average number of years at their residence when they enrolled in the study was reasonably long (15.1 years). Age strongly predicted duration at current residence but was not related to the number of lifetime residences. After adjusting for age, California-born women and women living in high socioeconomic status (SES) neighborhoods were significantly more residentially stable. Agreement between self-reported urbanization of recent residences and that based on census data of the geocoded residences was very good (80% concordant). Among women currently living in urban areas, an average of 43.3 years, or 77%, of their lifetimes were spent in urban residences; among women currently living in a rural area, an average of 37.3 years, or 67% of their lifetimes were spent in rural residences. CONCLUSIONS: This suggests that analyses of incidence rates based on current residence, while not capturing a woman's full exposure history, may reasonably reflect some aspect of longer term chronic exposures, especially those related to urbanization, at least in professional women.

Adult↗

Alcohol consumption and risk of non-Hodgkin lymphoma: a pooled analysis.

BACKGROUND: Previous epidemiological studies of the relation between alcohol consumption and risk of non-Hodgkin lymphoma (NHL) have been inconsistent, probably because of small sample sizes of individual studies that result from stratification by NHL subtype and type of alcoholic beverage. We aimed to assess the role of alcohol consumption in NHL with sufficient sample size to analyse by both type of alcoholic beverage and disease subtype. METHODS: We obtained original data from nine case-control studies from the USA, UK, Sweden, and Italy in the International Lymphoma Epidemiology Consortium (InterLymph), yielding a pooled study population of 15 175 individuals (6492 cases and 8683 controls). We derived odds ratios (OR) and 95% CI from unconditional logistic regression models, controlling for study centre and other confounding factors. Heterogeneity between studies was assessed by comparison of results from joint fixed-effects logistic regression and two-stage random-effects logistic regression, and by calculation of Wald chi(2) statistics. FINDINGS: People who drank alcohol had a lower risk of NHL than did non-drinkers (OR 0.83 [95% CI 0.76-0.89]). Compared with non-drinkers, risk estimates were lower for current drinkers than for former drinkers (0.73 [0.64-0.84] vs 0.95 [0.80-1.14]), but risk did not decrease with increasing alcohol consumption. The protective effect of alcohol did not vary by beverage type, but did change with NHL subtype. The lowest risk estimates were recorded for Burkitt's lymphoma (0.51 [0.33-0.77]). INTERPRETATION: People who drink alcoholic beverages might have a lower risk of NHL than those who do not, and this risk might vary by NHL subtype. Further study designs are needed to determine whether confounding lifestyle factors or immunomodulatory effects of alcohol explain this association.

Adolescent↗

Obesity, recreational physical activity, and risk of pancreatic cancer in a large U.S. Cohort.

BACKGROUND: Obesity and physical activity, in part through their effects on insulin sensitivity, may be modifiable risk factors for pancreatic cancer. METHODS: The authors analyzed data from the American Cancer Society Cancer Prevention Study II Nutrition Cohort to examine the association between measures of adiposity, recreational physical activity, and pancreatic cancer risk. Information on current weight and weight at age 18, location of weight gain, and recreational physical activity were obtained at baseline in 1992 via a self-administered questionnaire for 145,627 men and women who were cancer-free at enrollment. During the 7 years of follow-up, 242 incident pancreatic cancer cases were identified among these participants. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) and to adjust for potential confounding factors including personal history of diabetes and smoking. RESULTS: We observed an increased risk of pancreatic cancer among obese [body mass index (BMI) >/= 30] men and women compared with men and women of normal BMI [<25; RR, 2.08; 95% confidence interval (95% CI), 1.48-2.93, P(trend) = 0.0001]. After adjustment for between BMI, risk of pancreatic cancer was independently increased among men and women who reported a tendency for central weight gain compared with men and women reporting a tendency for peripheral weight gain (RR, 1.45; 95% CI, 1.02-2.07). We observed no difference in pancreatic cancer incidence rates between men and women who were most active (>31.5 metabolic equivalent hours per week) at baseline compared with men and women who reported no recreational physical activity (RR, 1.20; 95% CI, 0.63-2.27). CONCLUSION: This study, along with several recent studies, supports the hypothesis that obesity and central adiposity are associated with pancreatic cancer risk.

Aged↗

Cigarette smoking and risk of non-Hodgkin lymphoma: a pooled analysis from the International Lymphoma Epidemiology Consortium (interlymph).

BACKGROUND: The International Lymphoma Epidemiology Consortium (InterLymph) provides an opportunity to analyze the relationship between cigarette smoking and non-Hodgkin lymphoma with sufficient statistical power to consider non-Hodgkin lymphoma subtype. The results from previous studies of this relationship have been inconsistent, likely due to the small sample sizes that arose from stratification by disease subtype. To clarify the role of cigarette smoking in the etiology of non-Hodgkin lymphoma, we conducted a pooled analysis of original patient data from nine case-control studies of non-Hodgkin lymphoma conducted in the United States, Europe, and Australia. METHODS: Original data were obtained from each study and uniformly coded. Risk estimates from fixed-effects and two-stage random-effects models were compared to determine the impact of interstudy heterogeneity. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived from unconditional logistic regression models, controlling for study center, age, sex, and race. RESULTS: In our pooled study population of 6,594 cases and 8,892 controls, smoking was associated with slightly increased risk estimates (OR, 1.07; 95% CI, 1.00-1.15). Stratification by non-Hodgkin lymphoma subtype revealed that the most consistent association between cigarette smoking and non-Hodgkin lymphoma was observed among follicular lymphomas (n = 1452). Compared with nonsmokers, current smokers had a higher OR for follicular lymphoma (1.31; 95% CI, 1.12-1.52) than former smokers (1.06; 95% CI, 0.93-1.22). Current heavy smoking (> or = 36 pack-years) was associated with a 45% increased OR for follicular lymphoma (1.45; 95% CI, 1.15-1.82) compared with nonsmokers. CONCLUSIONS: Cigarette smoking may increase the risk of developing follicular lymphoma but does not seem to affect risk of the other non-Hodgkin lymphoma subtypes we examined. Future research is needed to determine the biological mechanism responsible for our subtype-specific results.

Adult↗

Relationship of obesity and physical activity with C-peptide, leptin, and insulin-like growth factors in breast cancer survivors.

INTRODUCTION: Obese and physically inactive breast cancer patients may have poorer survival compared with lighter weight and more active women. Several obesity-related and physical activity-related hormones and peptides may explain this association, including insulin, leptin, insulin-like growth factor-I (IGF-I), and IGF-binding protein-3. Few studies have examined the associations between obesity, physical activity, and these hormones/peptides among breast cancer survivors. PURPOSE: To determine whether obesity and physical activity are associated with insulin, IGFs, and leptin levels in a population-based sample of 710 women diagnosed with in situ to stage IIIA breast cancer and enrolled in the Health, Eating, Activity, and Lifestyle Study. METHODS: We collected a blood sample and information on physical activity among women diagnosed 2 to 3 years earlier using an interview-administered questionnaire. Trained staff measured weight. C-peptide, leptin, and IGFs were assayed by RIA. Mean hormone levels within body mass index and physical activity categories were adjusted for confounders using analysis of covariance methods. RESULTS: We observed higher C-peptide (P for trend = 0.0001) and leptin (P for trend = 0.0001) levels and lower IGF-I levels (P for trend = 0.0001) with higher levels of body mass index. We observed lower C-peptide (P for trend = 0.001) and leptin (P for trend = 0.001) levels and higher IGF-I (P for trend = 0.0037) and IGF-binding protein-3 (P for trend = 0.055) levels with higher levels of physical activity. CONCLUSIONS: Increasing physical activity and decreasing body fat may be a reasonable intervention approach toward changing insulin and leptin, thereby potentially influencing breast cancer prognosis.

Adult↗

Stroke risk and tamoxifen therapy for breast cancer.

BACKGROUND: Tamoxifen, which is used widely to treat, and increasingly to prevent, breast cancer, has been associated with increased risk of stroke. We assessed the impact of tamoxifen treatment for breast cancer on the risk of stroke, considering dose, duration, and recency of use of tamoxifen and known stroke risk factors. METHODS: We conducted a nested case-control study of stroke after breast cancer among female Los Angeles County residents enrolled in a large health maintenance organization when diagnosed with breast cancer between January 1, 1980, and July 1, 2000. We obtained information on breast cancer treatment and stroke risk factors through medical record review and telephone interviews. The association (odds ratio [OR] and 95% confidence interval [CI]) between tamoxifen and stroke risk was determined by using a conditional logistic regression model, adjusting for menopausal status and history of hypertension and diabetes. All statistical tests were two-sided. RESULTS: Of 11 045 women with breast cancer, 179 met stroke eligibility criteria and were individually matched to two stroke-free control subjects with breast cancer on age and year of breast cancer diagnosis. The mean age at breast cancer diagnosis was 66.6 years (standard deviation [SD] = 12.3 years), and the mean at-risk period (i.e., the time between breast cancer diagnosis and first stroke or comparable time period for control subjects) was 5.7 years (SD = 4.5 years). Tamoxifen use was not associated with risk of stroke, either overall (OR = 1.0, 95% CI = 0.6 to 1.6) or in subgroups defined by duration, dose, or recency of use. Chemotherapy, but not a specific chemotherapy regimen, was associated with an increased risk of stroke, regardless of tamoxifen use (no tamoxifen use, OR = 2.8, 95% CI = 1.3 to 6.3; tamoxifen use OR = 2.2, 95% CI = 1.2 to 4.1). CONCLUSIONS: Tamoxifen use is not associated with increased stroke risk. Further exploration of possible increased stroke risk following chemotherapy treatment for breast cancer is needed.

Adult↗

Nutrition and physical activity and chronic disease prevention: research strategies and recommendations.

A shortage of credible information exists on practical dietary and physical activity patterns that have potential to reverse the national obesity epidemic and reduce the risk of major cancers and other chronic diseases. Securing such information is a challenging task, and there is considerable diversity of opinion concerning related research designs and priorities. Here, we put forward some perspectives on useful methodology and infrastructure developments for progress in this important area, and we list high-priority research topics in the areas of 1) assessment of nutrient intake and energy expenditure; 2) development of intermediate outcome biomarkers; 3) enhancement of cohort and cross-cultural studies; and 4) criteria for and development of full-scale nutrition and physical activity intervention trials.

Biomarkers↗

Serum high-density lipoprotein cholesterol, metabolic profile, and breast cancer risk.

BACKGROUND: The prevalence of metabolic syndrome (obesity, glucose intolerance, low serum high-density lipoprotein cholesterol [HDL-C], high serum triglycerides, hypertension) is high and increasing in parallel with an increasing breast cancer incidence worldwide. HDL-C represents an important aspect of the syndrome, yet its role in breast cancer is still undefined. METHODS: In two population-based screening surveys during 1977-1983 and 1985-1987, serum HDL-C was assayed enzymatically among 38,823 Norwegian women aged 17-54 years at entry. Height, weight, blood pressure, serum lipids, fat and energy intake, physical activity, parity, oral contraceptive use, hormone therapy use, alcohol intake, and tobacco use were also assessed. We used Cox proportional hazards modeling to estimate the relative risk (RR) of breast cancer associated with serum HDL-C levels and to adjust for potential confounding variables. We performed stratified analyses to evaluate effect modification by body mass index (BMI) and menopausal status. All statistical tests were two-sided. RESULTS: During a median follow-up of 17.2 years, we identified 708 cases of invasive breast cancer. In multivariable analysis, the risk of postmenopausal breast cancer was inversely related to quartile of HDL-C (P(trend) =.02). Among women with HDL-C above 1.64 mmol/L (highest quartile) versus below 1.20 mmol/L (lowest quartile), the relative risk was 0.75 (95% confidence interval [CI] = 0.58 to 0.97). The HDL-C association was confined to women in the heavier subgroup (BMI > or =25 kg/m2), for whom the relative risk of postmenopausal breast cancer in those with HDL-C above 1.64 mmol/L versus below 1.20 mmol/L was 0.43 (95% CI = 0.28 to 0.67; P(trend)<.001; P(interaction) =.001). CONCLUSION: Low HDL-C, as part of the metabolic syndrome, is associated with increased postmenopausal breast cancer risk.

Adolescent↗

Reproductive factors and risk of breast carcinoma in a study of white and African-American women.

BACKGROUND: Few studies have investigated the association between reproductive factors and the risk of breast carcinoma among African-American women. The authors assessed whether the number of full-term pregnancies, age at first full-term pregnancy, and total duration of breastfeeding were associated with similar relative risk estimates in white and African-American women in a large multicenter, population-based case-control study of breast carcinoma. METHODS: Case patients were 4567 women (2950 white women and 1617 African-American women) ages 35-64 years with newly diagnosed invasive breast carcinoma between 1994 and 1998. Control patients were 4668 women (3012 white women and 1656 African-American women) who were identified by random-digit dialing and were frequency matched to case patients according to study center, race, and age. Adjusted odds ratios and 95% confidence intervals were estimated using unconditional logistic regression. RESULTS: For white women, the reduction in risk of breast carcinoma per full-term pregnancy was 13% among younger women (ages 35-49 years) and 10% among older women (ages 50-64 years). The corresponding risk reductions for African-American women were 10% and 6%, respectively. Risk decreased significantly with increasing number of full-term pregnancies for both races and both age categories. Duration of lactation was inversely associated with breast carcinoma risk among younger parous white (trend P = 0.0001) and African-American (trend P = 0.01) women. African-American women tended to have more children compared with white women, but parity rates were lower in younger women than in older women in both racial groups. However, breastfeeding was substantially more common in young white women than in young African-American women. CONCLUSIONS: Overall, parity and lactation had similar effects on breast carcinoma risk in white and African-American women. If younger African-American women now are giving birth to fewer children than in the past, without a substantial increase in breastfeeding, breast carcinoma rates may continue to increase at a more rapid rate among these women compared with white women.

Adult↗

Impact of reproductive factors and lactation on breast carcinoma in situ risk.

Incidence rates for breast carcinoma in situ (CIS) have increased markedly over the past 20 years. Breast CIS, detected primarily on mammography, now represents 30-45% of all screened detected breast cancers. We conducted a large population-based case-control study to evaluate the impact of reproductive factors and lactation on breast CIS risk. Case subjects were newly diagnosed with breast CIS at ages 35-64 years between March 1, 1995 and May 31, 1998 (n = 567), resided in Los Angeles County and were born in the United States. Control subjects (n = 614), identified through random digit dialing, fulfilled the same eligibility criteria and were required to have had at least one screening mammogram in the 2-year period before their interview. Women with a positive family history of breast cancer had a 2-fold increase in breast CIS risk. Parous women were at reduced risk relative to nulligravid women (odds ratio [OR] = 0.67, 95% confidence interval [CI] = 0.46-1.00). Among nulliparous women, pregnancy was unrelated to breast CIS risk. Among parous women, risk declined with each additional term pregnancy (p-trend = 0.003). No associations were found with age at first term pregnancy, induced abortion or miscarriage. Long duration of breast-feeding (> or =24 months) was associated with increased risk (OR = 2.00, 95% CI = 1.11-3.60). The observed effects of family history and pregnancy on breast CIS risk are consistent with those observed for invasive breast cancer. The results for breast-feeding are contrary to what has been observed in studies of invasive breast cancer.

Adult↗

Study design: evaluating gene-environment interactions in the etiology of breast cancer - the WECARE study.

INTRODUCTION: Deficiencies in cellular responses to DNA damage can predispose to cancer. Ionizing radiation can cause cluster damage and double-strand breaks (DSBs) that pose problems for cellular repair processes. Three genes (ATM, BRCA1, and BRCA2) encode products that are essential for the normal cellular response to DSBs, but predispose to breast cancer when mutated. DESIGN: To examine the joint roles of radiation exposure and genetic susceptibility in the etiology of breast cancer, we designed a case-control study nested within five population-based cancer registries. We hypothesized that a woman carrying a mutant allele in one of these genes is more susceptible to radiation-induced breast cancer than is a non-carrier. In our study, 700 women with asynchronous bilateral breast cancer were individually matched to 1400 controls with unilateral breast cancer on date and age at diagnosis of the first breast cancer, race, and registry region, and counter-matched on radiation therapy. Each triplet comprised two women who received radiation therapy and one woman who did not. Radiation absorbed dose to the contralateral breast after initial treatment was estimated with a comprehensive dose reconstruction approach that included experimental measurements in anthropomorphic and water phantoms applying patient treatment parameters. Blood samples were collected from all participants for genetic analyses. CONCLUSIONS: Our study design improves the potential for detecting gene-environment interactions for diseases when both gene mutations and the environmental exposures of interest are rare in the general population. This is particularly applicable to the study of bilateral breast cancer because both radiation dose and genetic susceptibility have important etiologic roles, possibly by interactive mechanisms. By using counter-matching, we optimized the informativeness of the collected dosimetry data by increasing the variability of radiation dose within the case-control sets and enhanced our ability to detect radiation-genotype interactions.

Adult↗

Polymorphism in the androgen receptor and mammographic density in women taking and not taking estrogen and progestin therapy.

There is some evidence that women with a higher number of CAG repeat lengths on the androgen receptor (AR) gene have increased breast cancer risk. We evaluated the association between AR-CAG repeat length and mammographic density, a strong breast cancer risk factor, in 404 African-American and Caucasian breast cancer patients. In postmenopausal estrogen progestin therapy users, carriers of the less active AR-CAG had statistically significantly higher mean percentage of density (41.4%) than carriers of the more active AR-CAG (25.7%; P = 0.04). Our results raise the question of whether the number of AR-CAG repeats predicts breast cancer risk in estrogen progestin therapy users.

Adult↗

Does mammographic density reflect ethnic differences in breast cancer incidence rates?

Breast cancer incidence rates in the United States are substantially lower among Asian-American women than among White or African-American women. The authors determined whether mammographic density reflects these ethnic differences by evaluating mammograms from 442 White, African-American, and Asian-American women without breast cancer who served as controls in one of two population-based, breast cancer case-control studies conducted in Los Angeles, California, in 1994-1998. Absolute and percent mammographic densities were determined with a previously developed and validated computer-assisted method. Data were analyzed using multiple regression methods. Mean age-adjusted percent mammographic density was significantly higher in Asian Americans (35.9%) than in African Americans (27.8%, p < 0.05) but was no longer significant after further adjustment for body mass index. After adjustment for age, body mass index, selected menstrual/reproductive factors, and family history, absolute mammographic density was statistically significantly lower in Asian Americans than in African Americans (p < 0.05) but not than in Whites. The ethnic difference in absolute mammographic density was particularly evident among women older than age 50 years. Additional adjustment for breast size reduced these ethnic differences. This study suggests that absolute but not percent mammographic density reflects the lower breast cancer incidence rates of Asian Americans in relation to those of African Americans and Whites.

Adult↗