有机氯农药及谷胱甘肽转移酶M1基因多态性与乳腺癌关系的研究

目的 研究血清中有机氯农药水平及谷胱甘肽转移酶M1(GSTM1)基冈多态性对女性乳腺癌患病风险的交互作用.方法 自2006年9月至2007年10月,在唐山市5所二甲以上医院收集经病理学确诊的乳腺癌患者70例.选取病例所在医院同期住院的女性患者,年龄相差不超过2岁,按相近居住地Ⅸ进行1:1配比作为对照.采用气相色谱-电子捕获(GC-ECD)方法检测血清中有机氯农药[滴滴涕(DDT)包括4种同分异构体:P,P'DDE、P,P'DDT、o,p'DDT、P,P'-DDD;六六六(HCH)包括4种同分异构体:α-HCH、β-HCH、γ-HCH、δ-HCH]残留水平,采用聚合酶链反应(PCR)检测GSTMl基因多态性,根据交互作用系数(γ)判断交互作用存在与否以及不同的基因.环境作用类型.结果 GSTM1基因多态性与DDT及HCH间存在一定的交互作用,交互作用系数分别为1.237、1.379,交互作用分别表现为次相乘模型和超相乘模型.结论 乳腺癌的发生是环境和遗传因素综合作用的结果.GSTM1基因多态性与环境危险因素DDT、HCH的暴露在乳腺癌发生中存在一定的交互作用.

Abstract：

Objective To study the potential effect of gene-environment interaction between glutathione S-transferase M1 (GSTM1) and serum organochlorines residues on the risk of breast cancer in women, in China. Methods Seventy newly pathologically diagnosed female patients with breast cancer from September 2006 to October 2007 were selected as the cases from five large hospitals in Tangshan. The controls were identified at the same hospital as cases. 1:1 matched case-control study. Between the cases and controls, the difference of age was not over two years and the residence was similar. The organochlorine residues levels in the serum were measured by gas chromatography (GC). Genotypes of GSTM1 polymorphisms were analyzed by multiplex allele-specific polymerase chain reaction (PCR). Interaction indexes (γ) were calculated to determine the type of gene-environment interaction. Results After confounding factors adjusted, the result showed that interaction existed in genetic polymorphisms of GSTM1 and DDT, HCH residues, and interaction indexes (γ) value were 1.237 and 1.379. Conclusion GSTM1 genetic polymorphisms and DDT, HCH may present an interaction in the development of breast cancer.     

Dietary Intake of B Vitamins and Methionine and Colorectal Cancer Risk

B vitamins are involved in 1-carbon metabolism, which is necessary for DNA replication, DNA repair, and regulation of gene expression. Recent studies suggest inverse associations between folate and vitamin B6 intakes and colorectal cancer risk but associations with other B vitamins and methionine have not been widely studied. After following 14,645 men and 22,467 women for 15 yr on average, we ascertained 910 incident colorectal cancers. Dietary intakes were estimated using a 121-item food frequency questionnaire. Hazard ratios (HRs) and 95% confidence intervals were estimated using Cox regression. We found some evidence of a U-shaped relationship between colon cancer risk and vitamin B6 and an inverse U-shaped relationship between rectal cancer risk and B12 (test for the quadratic trend, P = 0.005 and P = 0.0005 respectively). For colon cancer, we observed a reduced risk associated with low methionine/high folate, HR = 0.63 (0.49, 0.80) and an increased risk associated with high methionine/high folate, HR = 1.36 (1.06, 1.74) (P interaction < 0.0001). Our study suggests a U-shaped association between colon cancer risk and vitamin B6 intake and an inverse U-shaped association between rectal cancer risk and vitamin B12. Adequate folate intake might protect against colon cancer risk in those with low methionine intake.     

Dietary Methyl-Group Donor Intake and Breast Cancer Risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)

(1) Background: Methyl-group donors (MGDs), including folate, choline, betaine, and methionine, may influence breast cancer (BC) risk through their role in one-carbon metabolism; (2) Methods: We studied the relationship between dietary intakes of MGDs and BC risk, adopting data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort; (3) Results: 318,686 pre- and postmenopausal women were followed between enrolment in 1992–2000 and December 2013–December 2015. Dietary MGD intakes were estimated at baseline through food-frequency questionnaires. Multivariable Cox proportional hazards regression models were used to quantify the association between dietary intake of MGDs, measured both as a calculated score based on their sum and individually, and BC risk. Subgroup analyses were performed by hormone receptor status, menopausal status, and level of alcohol intake. During a mean follow-up time of 14.1 years, 13,320 women with malignant BC were identified. No associations were found between dietary intakes of the MGD score or individual MGDs and BC risk. However, a potential U-shaped relationship was observed between dietary folate intake and overall BC risk, suggesting an inverse association for intakes up to 350 µg/day compared to a reference intake of 205 µg/day. No statistically significant differences in the associations were observed by hormone receptor status, menopausal status, or level of alcohol intake; (4) Conclusions: There was no strong evidence for an association between MGDs involved in one-carbon metabolism and BC risk. However, a potential U-shaped trend was suggested for dietary folate intake and BC risk. Further research is needed to clarify this association.     

Association between Genetic Polymorphisms of N-acetyltransferase 2, Environmental Factors and Female Breast Cancer

目的 分析N-乙酰基转移酶-2( NAT2)基因多态性和环境因素与女性乳腺癌的关系.方法 采用以医院为基础的1:1配对的病例-对照研究,收集唐山市原发性乳腺癌新发女性患者48例与相应非肿瘤患者48例.以问卷调查收集各研究对象的饮食习惯和生活方式、生理生育、环境暴露和职业接触、既往病史、心理等信息.采用聚合酶链反应-限制性片段多态性(PCR-RFLP)技术检测NAT2的野生型等位基因WT、突变型等位基因M1、M2和M3突变频率,分析NAT2基因多态性和环境危险因素与女性乳腺癌的关系.结果 被动吸烟大于或等于10年(OR=3.957,95％CI:1.589～10.002)、居住地环境污染(OR=33.571,95％CI:4.270～263.967)、职业接触(OR=9.400,95％CI:1.127～78.405)、烹调时使用排油设备(OR=0.177,95％CI:0.060～0.529)、农药的使用(OR=28.200,95％CI:3.576～222.389)等是乳腺癌的环境危险因素.携带M2、M3等位基因可能是乳腺癌的危险因素,OR值分别为2.563(95％CI:1.155～5.707)和2.083(95％CI:1.068～4.062),而M1等位基因频率在病例组与对照组的分布差异无统计学意义(x2=0.447,P＞0.05).病例组与对照组突变杂合子基因型(WT/Mx)分布频率差异无统计学意义(x2=0.021,P＞0.05),而两组间突变纯合子(Mx/Mx)分布频率差异有统计学意义(OR=3.545,95％CI:1.141～11.015).慢乙酰化表型者患乳腺癌的风险是快乙酰化表型者的3.364倍(x2=7.599,P＜0.05).分层分析发现NAT2慢乙酰化表型与被动吸烟大于或等于10年存在交互作用(OR=9.917,95％CI:1.597～61.597).结论 NAT2基因多态性和部分环境危险因素与乳腺癌发病存在统计学关联.     

N-乙酰基转移酶-2基因多态性和环境因素与女性乳腺癌的关系

目的分析N-乙酰基转移酶-2(NAT2)基因多态性和环境因素与女性乳腺癌的关系。方法采用以医院为基础的1∶1配对的病例-对照研究,收集唐山市原发性乳腺癌新发女性患者48例与相应非肿瘤患者48例。以问卷调查收集各研究对象的饮食习惯和生活方式、生理生育、环境暴露和职业接触、既往病史、心理等信息。采用聚合酶链反应-限制性片段多态性(PCR-RFLP)技术检测NAT2的野生型等位基因WT、突变型等位基因M1、M2和M3突变频率,分析NAT2基因多态性和环境危险因素与女性乳腺癌的关系。结果被动吸烟大于或等于10年(OR=3.957,95%CI:1.589～10.002)、居住地环境污染(OR=33.571,95%CI:4.270～263.967)、职业接触(OR=9.400,95%CI:1.127～78.405)、烹调时使用排油设备(OR=0.177,95%CI:0.060～0.529)、农药的使用(OR=28.200,95%CI:3.576～222.389)等是乳腺癌的环境危险因素。携带M2、M3等位基因可能是乳腺癌的危险因素,OR值分别为2.563(95%CI:1.155～5.707)和2.083(95%CI:1.068～4.062),而M1等位基因频率在病例组与对照组的分布差异无统计学意义(χ2=0.447,P>0.05)。病例组与对照组突变杂合子基因型(WT/Mx)分布频率差异无统计学意义(χ2=0.021,P>0.05),而两组间突变纯合子(Mx/Mx)分布频率差异有统计学意义(OR=3.545,95%CI:1.141～11.015)。慢乙酰化表型者患乳腺癌的风险是快乙酰化表型者的3.364倍(χ2=7.599,P<0.05)。分层分析发现NAT2慢乙酰化表型与被动吸烟大于或等于10年存在交互作用(OR=9.917,95%CI:1.597～61.597)。结论 NAT2基因多态性和部分环境危险因素与乳腺癌发病存在统计学关联。     

Fruit,Vegetable, and Animal Food Intake and Breast Cancer Risk by Hormone Receptor Status

The effects of diet on breast cancer are controversial and whether the effects vary with hormone receptor status has not been well investigated. This study evaluated the associations of dietary factors with risk for breast cancer overall and by the hormone receptor status of tumors among Chinese women. The Shanghai Breast Cancer Study, a large, population-based, case-control study, enrolled 3,443 cases and 3,474 controls in 1996–1998 (phase I) and 2002–2005 (phase II); 2676 cases had estrogen receptor (ER) and progesterone receptor (PR) data. Dietary intake was assessed using a validated, quantitative, food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived from multivariate, polychotomous, unconditional logistic regression models. Total vegetable intake was inversely related to breast cancer risk, with an adjusted OR for the highest quintile of 0.80 (95% CI = 0.67–0.95; P trend = 0.02). Reduced risk was also related to high intake of allium vegetables (P trend = 0.01) and fresh legumes (P trend = 0.0008). High intake of citrus fruits and rosaceae fruits were inversely associated with breast cancer risk (P trend = 0.003 and 0.004, respectively), although no consistent association was seen for total fruit intake. Elevated risk was observed for all types of meat and fish intake (all P trend < 0.05), whereas intakes of eggs and milk were associated with a decreased risk of breast cancer (both P trend <0.05). There was little evidence that associations with dietary intakes varied across the 4 tumor subtypes or between ER+/PR+ and ER-/PR- tumors (P for heterogeneity >0.05). Our results suggest that high intake of total vegetables, certain fruits, milk, and eggs may reduce the risk of breast cancer, whereas high consumption of animal-source foods may increase risk. The dietary associations did not appear to vary by ER/PR status.     

Dairy Products,Calcium Intake,and Breast Cancer Risk: A Case-Control Study in China

The results of dairy food consumption and breast cancer risk are conflicting, and their relationship has not previously been studied in China. The objective of this study is to examine the association between dairy products, calcium intake, and breast cancer risk among Chinese women. A hospital-based case-control study was conducted among Chinese women in the Guangdong province from June 2007 to August 2008. Four hundred and thirty-eight consecutively recruited cases with primary breast cancer were frequency-matched to 438 controls on age and residence. Dietary intake information was collected by interviewers using a validated food frequency questionnaire. Odds ratios (ORs) and 95% confidence interval (CI) were estimated using unconditional multiple logistic regression adjusted for various potential confounders. We observed a statistically significant inverse association of dietary calcium intake with breast cancer risk, with the adjusted OR (95% CI) of 0.35 (0.22–0.56) comparing the highest with the lowest quartile. No significant association was found between dairy products measured either by dry weight of dairy product or dairy product protein intake and breast cancer risk. Our study supports a protective effect of high intake of dietary calcium on breast cancer risk, and no association with dairy product intake.     

Genetic Variation Interacts with Selenium Exposure Regarding Breast Cancer Risk: Assessing Dietary Intake,Serum Levels and Genetically Elevated Selenium Levels

Selenium has been suggested to be protective regarding breast cancer risk but no overall effect has been established. Genetics may modify the effect. This study compares the effect of selenium exposure on breast cancer risk between women with different alleles in single-nucleotide polymorphisms (SNPs). The Malmö Cancer and Diet Study, a cohort including 17,035 women and >25 years of follow-up on breast cancer diagnosis, was used. Five promising SNPs regarding interaction with selenium exposure were selected from the literature: rs1050450, rs4880, rs3877899, rs7579, and rs71304. Selenium exposure was assessed in three ways: genetically elevated (n = 16,429), dietary intake (n = 15,891) and serum levels (n = 2037) at baseline. Cox regression and logistic regression analyses evaluated breast cancer risk from selenium exposure, stratified for the SNPs and adjusted for risk factors. A total of 1946 women were diagnosed with breast cancer. Women with T/T alleles in rs1050450 had lower breast cancer risk compared with C/C, HR 0.81 (0.68–0.96). Interaction by rs1050450 limited a protective effect of higher selenium intake to T/T carriers, HR 0.68 (0.43–1.08) for intermediate intake and HR 0.63 (0.40–1.00) for high intake. No interactions or risk differences were seen for other SNPs or for serum selenium or genetically elevated selenium. The results indicate that genetic variation in rs1050450 might affect breast cancer risk and that selenium exposure could be a possible modifiable risk factor for breast cancer among women with that variation.     

BRCA1 Polymorphisms and Breast Cancer Epidemiology in the Western New York Exposures and Breast Cancer (WEB) Study

Results of studies for the association of BRCA1 genotypes and haplotypes with sporadic breast cancer have been inconsistent. Therefore, a candidate single nucleotide polymorphism (SNP) approach was used in a breast cancer case‐control study to explore genotypes and haplotypes that have the potential to affect protein functions or levels. In a breast cancer case‐control study, genotyping of BRCA1 polymorphisms Q356R, D693N, and E1038G was performed on 1,005 cases and 1,765 controls. Unconditional, polytomous logistic regression and χ²‐tests were used to examine the associations of breast cancer with genotypes and haplotypes. In addition, interactions between genotype and smoking, benign breast disease, family history of breast cancer, body mass index (BMI), alcohol consumption, and hormonal risk factors, hormone receptor status, and breast cancer pathology were calculated also using logistic regression and χ². Although sporadic breast cancer was not associated with BRCA1 genotypes or haplotypes overall or by menopausal status, there was evidence of an interaction between the E1038G BRCA1 genotype, smoking, and BMI among premenopausal women (P for interaction = 0.01 and 0.045, respectively) and between E1038G and D693N BRCA1 genotypes and hormone therapy use among postmenopausal women (P for interaction = 0.01 and 0.02, respectively). There were no other associations found between BRCA1 genotypes and stage, histological grade, or nuclear grade. However, the D693N SNP was associated with the risk of triple negative breast cancer (odds ratio = 2.31 95% confidence interval 1.08–4.93). The BRCA1 variants studied may play a role in the etiology of triple negative breast cancer and may interact with environmental factors such as hormone therapy or smoking and increase sporadic breast cancer risk.     

Does a High Folate Intake Increase the Risk of Breast Cancer?

Although not uniformly consistent, epidemiologic studies generally suggest an inverse association between dietary intake and blood measurements of folate and breast cancer risk. However, the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening trial has recently reported for the first time a potential harmful effect of high folate intake on breast cancer risk. In this study, the risk of developing breast cancer was significantly increased by 20% in women reporting supplemental folic acid intake ≥ 400 μg/d compared with those reporting no supplemental intake. Furthermore, although food folate intake was not significantly related to breast cancer risk, total folate intake, mainly from folic acid supplementation, significantly increased breast cancer risk by 32%. The data from the PLCO trial support prior observations made in epidemiologic, clinical, and animal studies suggesting that folate possesses dual modulatory effects on the development and progression of cancer depending on the timing and dose of folate intervention. Based on the lack of compelling supportive evidence, routine folic acid supplementation should not be recommended as a chemopreventive measure against breast cancer at present.     

Nitrate Intake Relative to Antioxidant Vitamin Intake Affects Gastric Cancer Risk: A Case-Control Study in Korea

The objective of this study was to determine whether the intake of nitrate relative to antioxidant vitamin rather than absolute intake of nitrate affects the risk of gastric cancer (GC). In a case-control study in Korea using a food frequency questionnaire, trained dietitians interviewed 136 GC cases and an equal number of controls matched by sex and age. As an index of nitrate intake relative to antioxidant vitamins intake, we calculated the nitrate:antioxidant vitamin consumption ratio. The mean daily nitrate intake from foods was very high in our subjects. Higher absolute intake of nitrate was not associated with GC risk [odds ratios (OR) = 1.13; 95% confidence interval (CI) = 0.42–3.06]. However, the GC risk distinctly increased as the nitrate:antioxidant vitamin consumption ratio increased, particularly with higher nitrate:vitamin E (OR = 2.78; 95% CI = 1.01–7.67) and nitrate:folate ratios (OR = 3.37; 95% CI = 1.28–8.87). Therefore, GC risk was influenced by the intake of nitrate relative to antioxidant vitamins. Our results suggest that a decrease in the intake of nitrate relative to antioxidant vitamins is considerably more effective in reducing GC risk than either a lower absolute intake of nitrate or a higher intake of antioxidant vitamins alone.     

Factors to Consider in the Association Between Soy Isoflavone Intake and Breast Cancer Risk

It has been suggested that soy isoflavones have protective effects against breast cancer. However, data from epidemiological studies are not conclusive. A recent meta-analysis showed that soy intake was inversely associated with breast cancer risk in Asian but not Western populations, which indicates that protection against breast cancer may require that women consume levels of soy typical in Asian diets. In addition to the amount of soy isoflavones consumed, the form and food source of isoflavones, timing of isoflavone exposure, estrogen receptor status of tumors, and equol-producer status and hormonal profile of individuals may modify the association between soy isoflavone intake and the risk of breast cancer. These factors might explain the heterogeneity of results from studies. This present report contrasts background data from Japanese and Western women to identify the potential modifying of these factors.Key words: breast cancer, soy isoflavones, review     

Dietary Mushroom Intake and the Risk of Breast Cancer Based on Hormone Receptor Status

Although many studies have documented the antitumor activities of mushrooms, the association between mushroom intake and breast cancer, defined by hormone receptor status, has received minimal empirical investigation. This study evaluated the association between mushroom intake and the risk of breast cancer according to hormone receptor status among Korean women. Mushroom intake and breast cancer risk were examined among 358 breast cancer patients and 360 cancer-free controls. Intake of mushrooms was assessed using a quantitative food frequency questionnaire. Greater mushroom intake was related to lower risk of breast cancers among premenopausal women (odds ratio [OR] = 0.35, 95% confidence interval [CI] = 0.13–0.91 for the highest vs. the lowest quartile intake). The association was stronger for premenopausal women with estrogen receptor (ER)+/progesterone receptor (PR) + tumors (OR = 0.30, 95% CI = 0.11–0.79 for the highest vs. the lowest quartile intake) than those with ER–/PR– tumors. Our results suggest that high consumption of mushrooms might be related to lower risks for breast cancers among premenopausal women; this association may be more robust among women with hormone receptor positive tumors.     

Combined Genetic and Nutritional Risk Models of Triple Negative Breast Cancer

Triple negative breast cancer (TNBC) presents clinical challenges due to unknown etiology, lack of treatment targets, and poor prognosis. We examined combined genetic and nutritional risk models of TNBC in 354 breast cancer cases. We evaluated 18 DNA-repair nonsynonymous single nucleotide polymorphisms (nsSNPs) and dietary/nutritional intakes. Multivariate Adaptive Regression Splines models were used to select nutrients of interest and define cut-off values for logistic regression models. Our results suggest that TNBC was associated with 6 DNA-repair nsSNPs, ERCC4 R415Q (rs1800067), MSH3 R940Q (rs184967), MSH6 G39E (rs1042821), POLD1 R119H (rs1726801), XRCC1 R194W (rs1799782), and XPC A499V (rs2228000) and/or deficiencies in 3 micronutrients (zinc, folate, and β-carotene). Combined analyses of these 6 nsSNPs and 3 micronutrients showed significant association with TNBC: odds ratios = 2.77 (95% confidence interval = 1.01–7.64) and 10.89 (95% confidence interval = 3.50–33.89) for 2 and at least 3 risk factors, respectively. To the best of our knowledge, this is the first study to suggest that multiple genetic and nutritional factors are associated with TNBC, particularly in combination. Our findings, if validated in larger studies, will have important clinical implication that dietary modulations and/or micronutrient supplementations may prevent or reverse TNBC phenotype, so tumors can be treated with less toxic therapeutic strategies, particularly in genetically susceptible women.     

Red and Processed Meat Intake,Polygenic Risk Score,and Colorectal Cancer Risk

High red and processed meat intake (RPMI) is an established risk factor for colorectal cancer (CRC). We aimed to assess the impact of RPMI on CRC risk according to and in comparison with genetically determined risk, which was quantified by a polygenic risk score (PRS). RPMI and potential confounders (ascertained by questionnaire) and a PRS (based on 140 CRC-related loci) were obtained from 5109 CRC cases and 4134 controls in a population-based case–control study. Associations of RPMI with CRC risk across PRS levels were assessed using logistic regression models and compared to effect estimates of PRS using “genetic risk equivalent” (GRE), a novel metric for effective risk communication. RPMI multiple times/week, 1 time/day, and >1 time/day was associated with 19% (95% CI 1% to 41%), 41% (18% to 70%), and 73% (30% to 132%) increased CRC risk, respectively, when compared to RPMI ≤ 1 time/week. Associations were independent of PRS levels (p_interaction = 0.97). The effect of RPMI > 1 time/day was equivalent to the effect of having 42 percentiles higher PRS level (GRE 42, 95% CI 20–65). RPMI increases CRC risk regardless of PRS levels. Avoiding RPMI can compensate for a substantial proportion of polygenic risk for CRC.     

Well-Done Meat Intake,Heterocyclic Amine Exposure,and Cancer Risk

High intake of meat, particularly red and processed meat, has been associated with an increased risk of a number of common cancers such as breast, colorectum, and prostate in many epidemiological studies. Heterocyclic amines (HCAs) are a group of mutagenic compounds found in cooked meats, particularly well-done meats. HCAs are some of most potent mutagens detected using the Ames/salmonella tests and have been clearly shown to induce tumors in experimental animal models. Over the past 10 years, an increasing number of epidemiological studies have evaluated the association of well-done meat intake and meat carcinogen exposure with cancer risk. The results from these epidemiologic studies were evaluated and summarized in this review. The majority of these studies have shown that high intake of well-done meat and high exposure to meat carcinogens, particularly HCAs, may increase the risk of human cancer.     

Long-term Dietary Acrylamide Intake and Breast Cancer Risk in a Prospective Cohort of Swedish Women

The association between dietary acrylamide intake and the incidenceof invasive breast cancer was examined among 61,433 Swedishwomen who were cancer free and completed a food frequency questionnairein 1987–1990 and again in 1997. During a mean follow-upof 17.4 years, a total of 2,952 incident cases of breast cancerwere diagnosed in the cohort. In multivariate analyses controllingfor breast cancer risk factors, no statistically significantassociation was observed between long-term acrylamide intake(assessed at baseline and in 1997) and the risk of breast cancer,overall or by estrogen receptor (ER) and progesterone receptor(PR) status. The multivariate rate ratios comparing extremequartiles of acrylamide intake were 0.91 (95% confidence interval(CI): 0.80, 1.02) for overall breast cancer, 0.89 (95% CI: 0.74,1.08) for ER+PR+ tumors, 1.17 (95% CI: 0.84, 1.64) for ER+PR–tumors, and 0.91 (95% CI: 0.61, 1.38) for ER–PR–tumors. The association between acrylamide intake and breastcancer risk did not differ by smoking status. These findingsfor Swedish women do not support the hypothesis that dietaryacrylamide is positively associated with risk of breast cancer,at least not within the ranges of acrylamide consumed by thispopulation. acrylamide; breast neoplasms; cohort studies; diet; prospective studies     

Dietary Vitamin D and Calcium Intake and Premenopausal Breast Cancer Risk in a German Case-Control Study

Epidemiological studies and laboratory data suggest that vitamin D may protect against the development of cancer, including breast cancer. Vitamin D supply affects the bioavailability of dietary calcium, which might also have anticarcinogenic effects. However, few studies considered them jointly. We used a population-based case-control study in Germany to examine the independent and joint effects of dietary vitamin D and calcium on premenopausal breast cancer risk. Dietary information was assessed using a validated food frequency questionnaire from 278 premenopausal cases and 666 age-matched controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multivariate models adjusting vitamin D models for calcium intake and vice versa. Breast cancer risk was significantly inversely associated with vitamin D intake. The OR and 95% CI for the highest intake category (≥ 5 μ g/day) was 0.50 (95% CI = 0.26–0.96) compared with the lowest (< 2 μ g/day; P_trend = 0.02). Dietary calcium intake was not associated with breast cancer (OR = 0.73, 95% CI = 0.41–1.29) for the highest (≥ 1,300 mg/day) versus the lowest category (< 700 mg/day), P_trend = 0.29). No statistically significant interaction between the 2 nutrients was observed. Our data support a protective effect of dietary vitamin D on premenopausal breast cancer risk independent of dietary calcium intake.     

Intake of Energy-Dense Foods,Fast Foods,Sugary Drinks,and Breast Cancer Risk in African American and European American Women

Limiting energy-dense foods, fast foods, and sugary drinks that promote weight gain is a cancer prevention recommendation, but no studies have evaluated intake in relation to breast cancer risk in African American (AA) women. In a case-control study with 1692 AA women (803 cases and 889 controls) and 1456 European American (EA) women (755 cases and 701 controls), odds ratios (OR) and 95% confidence intervals (CI) for risk were computed, stratifying for menopausal and estrogen receptor (ER) status. Among postmenopausal EA women, breast cancer risk was associated with frequent consumption of energy-dense foods (OR = 2.95; 95% CI: 1.66–5.22), fast foods (OR = 2.35; 95% CI: 1.38–4.00), and sugary drinks (OR = 2.05; 95% CI: 1.13–3.70). Elevated risk of ER+ tumors in EA women was associated with energy-dense (OR = 1.75; 95% CI: 1.14–2.69) and fast foods (OR = 1.84; 95% CI: 1.22–2.77). Among AA women, frequent fast food consumption was related to premenopausal breast cancer risk (OR = 1.97; 95% CI: 1.13–3.43), and with ER+ tumors. Energy adjustment attenuated risk estimates in AA women, while strengthening them among EA women. Frequent consumption of energy-dense and fast foods that have poor nutritive value appeared to increase breast cancer risk in AA and EA women, with differences by menopausal status and ER status.