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Heusinger K.,University Breast Center Franconia | Loehberg C.R.,University Breast Center Franconia | Haeberle L.,University Breast Center Franconia | Jud S.M.,University Breast Center Franconia | And 13 more authors.
European Journal of Cancer Prevention | Year: 2011

Mammographic percent density (MD) is recognized as one of the strongest risk factors associated with breast cancer. This matched case-control study investigated whether MD represents an independent risk factor. Mammograms were obtained from 1025 breast cancer patients and from 520 healthy controls. MD was measured using a quantitative computer-based threshold method (0-100%). Breast cancer patients had a higher MD than healthy controls (38 vs. 32%, P<0.01). MD was significantly higher in association with factors such as age over 60 years, body mass index (BMI) of 25-30 kg/m, nulliparity or low parity (one to two births). Average MD was inversely associated with age, BMI, parity and positively associated with age at first full-term pregnancy. MD was higher in women with at least one first-degree relative affected, but only among patients and not in the group of healthy controls (P<0.01/P=0.61). In women with an MD of 25% or more, the risk of breast cancer was doubled compared with women with an MD of less than 10% (odds ratio: 2.1; 95% confidence interval: 1.3-3.4; P<0.01); in the postmenopausal subgroup, the risk was nearly tripled (odds ratio: 2.7; 95% confidence interval: 1.6-4.7; P<0.001). This study provides further evidence that MD is an important risk factor for breast cancer. These results indicate strong associations between MD and the risk of breast cancer in a matched case-control study in Germany © 2010 Wolters Kluwer Health. Source


Loehberg C.R.,University Breast Center Franconia | Heusinger K.,University Breast Center Franconia | Jud S.M.,University Breast Center Franconia | Haeberle L.,University Breast Center Franconia | And 13 more authors.
European Journal of Cancer Prevention | Year: 2010

Mammographic density (MD) has consistently been found as one of the strongest breast cancer risk factors. In our study, both qualitative and quantitative density measurements were performed in a hospital-based group of premenopausal women before and after first full-term pregnancy providing an opportunity for direct evaluation of the effects of one pregnancy on MD. Mammograms were obtained from 23 women before and after first full-term pregnancy and from 28 nulliparous controls. MD was determined by a standard qualitative assessment method using the Breast Imaging Reporting and Data System, and a quantitative computer-based threshold method (0-100%). The mean age at mammography before and after pregnancy was 31 and 34 years, respectively, with a mean difference of 40 months between mammographies. The quantitative density assessment showed a significant reduction in relative MD after pregnancy of 12 percentage points (8.6-15.4), compared with 3.1 (0.0-6.2) in the nulliparous control group (P<0.001). A reduction in MD of more than 10% was seen in 52% of the patients, compared with 18% of the controls. The qualitative density assessment confirmed a reduction in MD after pregnancy by one Breast Imaging Reporting and Data System category (P=0.02). This longitudinal study showed that MD can be influenced by one full-term pregnancy. This effect was seen with both quantitative and qualitative assessment methods. It may be hypothesized that breast cancer risk reduction associated with pregnancy is mediated through a direct reduction of MD, and MD assessment might be incorporated in individualizing risk assessment and prevention. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source


Warren H.,London School of Hygiene and Tropical Medicine | Dudbridge F.,London School of Hygiene and Tropical Medicine | Fletcher O.,Institute of Cancer Research | Orr N.,Institute of Cancer Research | And 149 more authors.
Cancer Epidemiology Biomarkers and Prevention | Year: 2012

Background: Our recent genome-wide association study identified a novel breast cancer susceptibility locus at 9q31.2 (rs865686). Methods: To further investigate the rs865686-breast cancer association, we conducted a replication study within the Breast Cancer Association Consortium, which comprises 37 case-control studies (48,394 cases, 50,836 controls). Results: This replication study provides additional strong evidence of an inverse association between rs865686 and breast cancer risk [study-adjusted per G-allele OR, 0.90; 95% confidence interval (CI), 0.88; 0.91, P =2.01 × 10-29] among women of European ancestry. There were ethnic differences in the estimated minor (G)-allele frequency among controls [0.09, 0.30, and 0.38 among, respectively, Asians, Eastern Europeans, and other Europeans; P for heterogeneity (Phet) = 1.3 × 10-143], but no evidence of ethnic differences in per allele OR (Phet = 0.43). rs865686 was associated with estrogen receptor-positive (ER+) disease (per G-allele OR, 0.89; 95% CI, 0.86-0.91; P = 3.13 × 10-22) but less strongly, if at all, with ER-negative (ER+) disease (OR, 0.98; 95% CI, 0.94-1.02; P = 0.26; Phet = 1.16 × 10-6), with no evidence of independent heterogeneity by progesterone receptor or HER2 status. The strength of the breast cancer association decreased with increasing age at diagnosis, with case-only analysis showing a trend in the number of copies of theGallele with increasing age at diagnosis (P for linear trend = 0.0095), but only among women with ER+ tumors. Conclusions: This study is the first to show that rs865686 is a susceptibility marker for ER+ breast cancer. Impact: The findings further support the view that genetic susceptibility varies according to tumor subtype. ©2012 AACR. Source


Yang X.R.,U.S. National Institutes of Health | Chang-Claude J.,Institute of Cancer Research | Goode E.L.,German Cancer Research Center | Nevanlinna H.,Mayo Medical School | And 129 more authors.
Journal of the National Cancer Institute | Year: 2011

Background Previous studies have suggested that breast cancer risk factors are associated with estrogen receptor (ER) and progesterone receptor (PR) expression status of the tumors. Methods We pooled tumor marker and epidemiological risk factor data from 35568 invasive breast cancer case patients from 34 studies participating in the Breast Cancer Association Consortium. Logistic regression models were used in case-case analyses to estimate associations between epidemiological risk factors and tumor subtypes, and case-control analyses to estimate associations between epidemiological risk factors and the risk of developing specific tumor subtypes in 12 population-based studies. All statistical tests were two-sided. Results In case-case analyses, of the epidemiological risk factors examined, early age at menarche (≤12 years) was less frequent in case patients with PR- than PR+ tumors (P =. 001). Nulliparity (P = 3 × 10 -6) and increasing age at first birth (P = 2 × 10-9) were less frequent in ER- than in ER+ tumors. Obesity (body mass index [BMI] ≥ 30 kg/m2) in younger women (≤50 years) was more frequent in ER-/PR- than in ER +/PR+ tumors (P = 1 × 10-7), whereas obesity in older women (>50 years) was less frequent in PR- than in PR+ tumors (P = 6 × 10-4). The triple-negative (ER-/PR-/HER2-) or core basal phenotype (CBP; triple-negative and cytokeratins [CK]5/6+ and/or epidermal growth factor receptor [EGFR]+) accounted for much of the heterogeneity in parity-related variables and BMI in younger women. Case-control analyses showed that nulliparity, increasing age at first birth, and obesity in younger women showed the expected associations with the risk of ER+ or PR + tumors but not triple-negative (nulliparity vs parity, odds ratio [OR] = 0.94, 95% confidence interval [CI] = 0.75 to 1.19, P =. 61; 5-year increase in age at first full-term birth, OR = 0.95, 95% CI = 0.86 to 1.05, P =. 34; obesity in younger women, OR = 1.36, 95% CI = 0.95 to 1.94, P =. 09) or CBP tumors. Conclusion sThis study shows that reproductive factors and BMI are most clearly associated with hormone receptor-positive tumors and suggest that triple-negative or CBP tumors may have distinct etiology. © 2011 The Author. Source

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