Differences In Breast Cancer Rates Research Articles

The Many Faces of Obesity and Its Influence on Breast Cancer Risk.

Obesity is associated with increased risk of breast and other cancers. However, the complexity of the underlying mechanisms, together with the interplay of diet and physical activity—contributing to energy balance—and the role of adipose tissue, pose challenges to our understanding of the basis of this increased risk. Epidemiologic studies have documented a higher obesity prevalence in US black women compared to white women. Elucidation of the contribution of potential biological differences among racially distinct groups to their differences in breast cancer (BC) risk and mortality have been topics of considerable interest in recent years. The racial and ethnic variation in body fat distribution may account for at least part of the differences in breast cancer rates in these populations. Yet, while black women exhibit higher rates of obesity compared to white women, this does not translate directly into higher rates of BC. In fact, overall, BC in black women occurs with a lower incidence than BC in white women. Obesity is a known risk factor for postmenopausal breast cancer, and growing evidence suggests that abdominal obesity, also known as central obesity, may increase risk for triple negative breast cancer, which is more common in premenopausal women. The positive association of postmenopausal BC risk and specifically estrogen receptor (ER)-positive BC, is presumably due largely to accumulation of estrogen in the adipose tissue of the breast and other tissues. Of the two main types of adipose tissue—subcutaneous and visceral—visceral adipocytes are more active metabolically. Such adipose tissue harbors multiple molecular entities that promote carcinogenesis: endocrine molecules/hormones, immunologic factors, inflammatory cytokines, metabolic alterations, and other components of the microenvironment. Expression of these culpable entities is largely regulated by epigenetic mechanisms. The interrelationship between these entities and drivers of epigenetic alteration are critical to the regulation of pathways connecting obesity and cancer risk. Initiatives to counteract the carcinogenic effects of obesity have primarily involved modulation of energy balance by diet. However, targeting of specific molecular abnormalities characterizing adiposity offers an alternative approach to preventing cancer. Our goal in this review is to first discuss the major mechanisms contributing to the obesity-breast cancer link. We will also consider race, specifically black/white differences, as they relate to the association of obesity with breast cancer risk. Then we will enumerate strategies targeting these mechanisms to reduce BC risk, in large part by way of dietary interventions with potential to mitigate the cancer-promoting components of adiposity.

Endogenous Estrogens, Estrogen Metabolites, and Breast Cancer Risk in Postmenopausal Chinese Women

The role of estrogen metabolism in determining breast cancer risk and differences in breast cancer rates between high-incidence and low-incidence nations is poorly understood. We measured urinary concentrations of estradiol and estrone (parent estrogens) and 13 estrogen metabolites formed by irreversible hydroxylation at the C-2, C-4, or C-16 positions of the steroid ring in a nested case-control study of 399 postmenopausal invasive breast cancer case participants and 399 matched control participants from the population-based Shanghai Women's Health Study cohort. Odds ratios (ORs) and 95% confidence intervals (CIs) of breast cancer by quartiles of metabolic pathway groups, pathway ratios, and individual estrogens/estrogen metabolites were estimated by multivariable conditional logistic regression. Urinary estrogen/estrogen metabolite measures were compared with those of postmenopausal non-hormone-using Asian Americans, a population with three-fold higher breast cancer incidence rates. All statistical tests were two-sided. Urinary concentrations of parent estrogens were strongly associated with breast cancer risk (ORQ4vsQ1 = 1.94, 95% CI = 1.21 to 3.12, Ptrend = .01). Of the pathway ratios, the 2-pathway:total estrogens/estrogen metabolites and 2-pathway:parent estrogens were inversely associated with risk (ORQ4vsQ1 = 0.57, 95% CI = 0.35 to 0.91, Ptrend = .03, and ORQ4vsQ1 = 0.61, 95% CI = 0.37 to 0.99, Ptrend = .04, respectively). After adjusting for parent estrogens, these associations remained clearly inverse but lost statistical significance (ORQ4vsQ1 = 0.65, 95% CI = 0.39 to 1.06, Ptrend = .12 and ORQ4vsQ1 = 0.76, 95% CI = 0.44 to 1.32, Ptrend = .28). The urinary concentration of all estrogens/estrogen metabolites combined in Asian American women was triple that in Shanghai women. Lower urinary parent estrogen concentrations and more extensive 2-hydroxylation were each associated with reduced postmenopausal breast cancer risk in a low-risk nation. Markedly higher total estrogen/estrogen metabolite concentrations in postmenopausal United States women (Asian Americans) than in Shanghai women may partly explain higher breast cancer rates in the United States.

Understanding rural-urban differences in risk factors for breast cancer in an Indian population.

Although cancer registry data indicate that there are large differences in breast cancer (BC) rates between rural and urban regions of India, the reasons for these differences are not well understood. We conducted a hospital based case-control study (1,637 breast cancer cases; 1,515 visitor controls) in Mumbai, India, during the years 2009-2013. Extensive questionnaire data, anthropometry measurement and blood samples were collected on all participants. Using logistic regression models, we estimated risk based on odds ratio (OR) and 95 % confidence intervals (CI) for various reproductive and anthropometric measures, stratified by rural-urban status depending upon residence in first 20 years of life. Waist-to-hip ratio of ≥0.95 compared to ratio ≤0.84 was strongly associated with risk of BC in both rural and urban populations (ORurban = 4.10, 95 % CI 3.03-5.56; ORrural = 3.01, 95 % CI 1.85-4.90). First full-term pregnancy after the age of 25 compared to first full-term pregnancy below 20 years of age was associated with risk of BC in both urban and rural women (ORurban = 1.78, 95 % CI 1.32-2.41; ORrural = 2.24, 95 % CI 1.13-4.43). The prevalence of age at first full-term pregnancy was significantly lower in rural (mean age at first full-term pregnancy = 19.39 years) versus urban women (mean age at first full-term pregnancy = 22.62 years), whereas mean waist circumference was much higher in urban women (82.13 cm) compared to rural women (79.26 cm). We did not observe any association between breast feeding and risk of BC. Differences in the prevalence of central adiposity and age at first full-term pregnancy between rural and urban women from India may explain some differences in breast cancer rates between these two populations.

The frequency of BRCA1 founder mutation c.5266dupC (5382insC) in breast cancer patients from Ukraine.

Germ-line mutations in several genes, such as BRCA1 and BRCA2, are known to increase the risk of breast cancer. These heritable mutations are unequally represented among populations with different ethnic background due to founder effects and thereby contribute to differences in breast cancer rates in different populations. The BRCA1 mutation c.5266dupC (also known as 5382insC or 5385insC) was detected in a sample of 193 breast cancer patients in Ukraine by multiplex mutagenically separated PCR using published specific primers. Nine BRCA1 mutations 5382insC were detected (4.7 %). The difference in age of diagnosis (35 years in 5382insC carriers versus 45 years in non-carriers) we observed is consistent with other reports indicating that the 5382insC mutation is a factor of genetic predisposition to breast cancer, which is consistent with reports from other countries.

Abstract B89: Timeliness in follow-up after abnormal mammography screening among Asian groups

Abstract Background: Treatment of breast cancer at the earliest possible stage results from a combination of screening for non-palpable abnormalities and timely and appropriate follow-up of abnormal test results. Studies have addressed Black-White differences in follow-up of abnormal mammograms but little is known about other groups including Asian Americans, a population composed of distinct ethnic sub-groups with substantial heterogeneity in risk factors that correspond with important to differences in breast cancer rates. In this study we aimed to assess completion and timeliness of diagnostic follow-up after an abnormal mammogram between White and Asian women and among disaggregated Asian ethnic subgroups. Methods: Using data from the San Francisco Mammography Registry, we identified women with an index abnormal screening mammogram result of BIRADS 0/3+ between the years 2000-2010. Our study sample included women who self-report White or Asian race/ ethnicity, ages 40 and older. Our outcomes were: 1) proportion of women without diagnostic follow-up within a year of their index mammogram, and 2) median days to diagnostic follow-up. Results: We identified 54028 White and Asian women between 2000 and 2010 in the SFMR data. Seventy percent of women were White and 30% were Asians. Among Asians, 16.2% were Chinese, 6.7% Filipina, 1.8% Japanese, 1.1% Vietnamese, 2.4% Other Asian, and 1.4% Mixed Asian. The majority of women were between the ages of 40-59 (67%). A total of 6023 (11.1%) of women did not receive follow-up within one year after an index abnormal mammogram. A higher proportion of Asian women did not receive follow-up compared to Whites (15% vs 10%). Among Asian groups, Filipinas had the highest percentage of women not receiving follow-up (18%) while Japanese women had the lowest (10.4%). In comparisons of individuals who received follow-up to those who did not, a higher proportion of women with no follow-up had lower education levels (24% vs 15%). Median time to diagnostic follow-up for White and Asian women combined was 18 days. The median follow-up time was 15 days for Whites, and 26 days for Asians. Among Asians, the median follow-up time differed significantly among ethnic groups: Japanese women had the lowest (19 days) and Vietnamese women the longest (30 days) followed by Filipinas (28 days). Conclusion: We observed disparities in timeliness to follow-up between White and Asian women and among Asian ethnic groups. Disaggregation of ethnicity can identify subpopulations most in need of breast cancer control, and to provide more specific information on breast cancer patterns. Citation Format: Kim H. Nguyen, Leah Karliner, Rena J. Pasick. Timeliness in follow-up after abnormal mammography screening among Asian groups. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr B89. doi:10.1158/1538-7755.DISP13-B89

P83 Should children from HHT families undergo screening thoracic CT scans for the diagnosis of pulmonary arteriovenous malformations? Survey data on breast cancer incidence

BackgroundLimiting thoracic radiation burden is a driving force for development of diagnostics, with the use of childhood CT scans particularly linked to increased cancer incidence [1]. Imaging of children with...

Food, Beverage, and Macronutrient Intakes in Postmenopausal Caucasian and Chinese-Canadian Women

International differences in breast cancer rates and diet, and studies in migrants, suggest that diet may be a modifiable risk factor for breast cancer. The goal of this cross-sectional study was to examine the dietary intakes of women from populations considered to be at different risks for breast cancer. We collected four 24-h food recalls in 3 groups of postmenopausal Canadian women: Caucasians (n = 392), Chinese women born in the West or who migrated to the West before age 21 (n = 156), and recent Chinese migrants (n = 383). Compared to Caucasians, recent Chinese migrants had lower energy and fat intakes and higher protein and carbohydrate intakes. Recent Chinese migrants consumed higher amounts of grains, vegetables, fish, and soy and lower amounts of alcohol, meat, dairy products, and sweets than Caucasians. Western-born Chinese and early Chinese migrants had intakes intermediate between the other 2 groups. The differences in intake between the ethnic groups suggest foods and nutrients that may contribute to the differences in risk of breast cancer between women in Canada and China. Future work will examine whether these dietary differences are associated with biological markers of breast cancer risk.

The Women's Health Initiative: Implications for clinicians

The Women's Health Initiative (WHI), the largest and longest randomized controlled study to date of the effect of dietary change on disease outcomes in postmenopausal women, failed to show that a low-fat diet prevents breast cancer, colon cancer, or cardiovascular disease. However, as the authors point out, the WHI Extension Study provides opportunities to assess whether nearly significant differences in breast cancer rates at 8 years become significant after 10 years of follow-up.

Nutrition and Lifestyle Factors on the Risk of Developing Breast Cancer

Aspects of nutrition and lifestyle may be largely responsible for the development of common cancers in Western countries, as indicated by the large differences in breast cancer rates between countries, the striking changes in these rates among migrating populations, and the rapid changes over time within countries. The better informed and increasingly health-conscious population of the present day are intensively seeking to identify and eliminate these putative carcinogenic risk factors and to exploit the preventive effects that have been attributed to certain dietary components. Nutrition and 'lifestyle' may exert its carcinogenic effects indirectly by cell stimulations (alcohol, hormone therapy in postmenopause), inhibition of DNA-repair mechanisms (lack of vitamins), effecting estrogen metabolism (phytoestrogenes), or as promotors to enhance growth of tumours (body mass index). Some 'substances' may act as a carcinogenic itself, for example, aromatic hydrocarbons in tobacco or increased polycyclic aromatic hydrocarbons in well done meat. Individual differences in the effects of nutritional factors on mammary epithelia could be caused by genetic polymorphisms. In this critical review, we focus on current data regarding the effect of nutrition and lifestyle, on the risk of developing breast cancer. A health lifestyle, consisting of 'healthy diet', physical activity, renunciation of stimulants, is recommended from childhood throughout life.

Reduction of the risk of breast cancer

Aspects of nutrition and lifestyle may be largely responsible for the development of common cancers in Western countries, as indicated by the large differences in breast cancer rates between countries, the striking changes in these rates among migrating populations, and the rapid changes over time within countries. The better informed and increasingly health-conscious population of the present day are intensively seeking to identify and eliminate these putative carcinogenic risk factors and to exploit the preventive effects that have been attributed to certain dietary components. Nutrition and 'lifestyle' may exert its carcinogenic effects indirectly by cell stimulations (alcohol, hormone replacement therapy), inhibition of DNA-repair mechanisms (lack of vitamins), effecting estrogen metabolism (phytoestrogen), or as promotors to enhance growth of tumors (body mass index). Some 'substances' may act as a carcinogenic itself, e. g. aromatic hydrocarbons in tobacco or increased polycyclic aromatic hydrocarbons in well done meat. Individual differences in the effects of nutritional factors on mammary epithelia could be caused by genetic polymorphisms. In this critical review, we focus on current data regarding the effect of nutrition and lifestyle, on the risk of developing breast cancer. A health lifestyle, consisting of "healthy diet", physical activity, renunciation of stimulants, is recommended from childhood throughout life.

Socioeconomic status and breast cancer incidence in California for different race/ethnic groups.

The majority of research on breast cancer risk and socioeconomic status (SES) has been conducted for blacks and whites. This study evaluates the relationship between SES and breast cancer incidence in California for four race/ethnic groups. Principal component analysis was used to create an SES index using 1990 Census data. Untracted cases were randomly allocated to census block groups within their county of residence. A total of 97,227 female breast cancer cases diagnosed in California between 1988 and 1992 were evaluated. Incidence rates and rate ratios (RRs) were estimated and a chi2 test for trend across SES levels was performed. SES was positively related to breast cancer incidence, and this effect was stronger for Hispanics and Asian/others than for whites and blacks. Adjusting by SES did not eliminate the differences in breast cancer rates among race/ethnic groups. RR differences between the race/ethnic groups were greatest in the lowest SES category and attenuated with increasing SES. An increasing trend over SES was statistically significant for all race/ethnic groups. Including randomly allocated cases affected RR estimates for white women only. Our results are consistent with similar findings for the Los Angeles area but differ from previous results for the San Francisco Bay area.

Nutritional risk factors for breast cancer.

The observation of large differences in breast cancer rates between countries has led to the hypothesis that excessive intake of dietary fat is an important risk factor for breast cancer in women. Case-control and prospective studies, however, generally have failed to show associations between dietary fat and breast cancer risk. There therefore is only weak evidence that modest reductions in fat intake (for instance to levels of 30% of caloric intake from fat) will reduce breast cancer risk. The possible benefits of lowering fat intake to levels substantially below 30% of calories will need to be tested in a randomized trial. In the meantime, the possible roles of micronutrient imbalances and childhood nutritional factors need to be studied better. Obesity is related to breast cancer in a complex way that suggests that a hormonal correlate of excessive body weight might affect breast cancer growth and metastasis. The potential benefit of intentional weight loss as an adjunct breast cancer treatment deserves further study. Many studies have suggested that drinking alcohol, even at modest levels, might increase breast cancer risk. Because the potential benefits of modest levels of alcohol for cardiovascular disease may outweigh the risk for breast cancer, recommendations for total alcohol abstinence may be premature for women with an average breast cancer risk. Women at unusually high risk for breast cancer who have a lower-than-average risk for cardiovascular disease, however, might make an informed decision to abstain from alcohol intake. Following current dietary advice to increase the amount of fruits, vegetables, and whole grains in the diet while reducing fats is certainly prudent for women to reduce their risk of several chronic disease, but current data points to the somber conclusion that such changes probably will have little effect on breast cancer risk.