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Additional file 1: Supplementary Table S1. A body shape index in relation to breast cancer recurrence and mortality.

Zinc has been suggested to play a role in breast cancer progression; however, no previous study on zinc levels and the potential effect on breast cancer survival has been conducted. This study investigates recurrence-free survival (RFS), breast cancer-specific survival (BCSS) and overall survival (OS) in relation to zinc levels, in serum and diet, overall and stratified for phosphorus and selenium levels. The Malmö Diet and Cancer Study, a prospective population-based cohort in Sweden including 17,035 women, was used to identify breast cancer patients diagnosed in the period 1991–2013. Diet was assessed by a validated modified diet history method. A Cox regression analysis yielded hazard ratios (HRs) with 95% confidence intervals adjusted for potential confounders. Out of 1062 patients with invasive breast cancer, 268 recurrences, 205 breast cancer deaths and 228 deaths from other causes were recorded. No overall associations were seen between zinc and RFS, BCSS or OS. However, in women with a high phosphorus intake, a higher BCSS and OS were seen in zinc intake Q2 to Q4 versus Q1; the adjusted HR was 0.41 (0.23–0.73) and 0.64 (0.41–1.00), respectively. The results indicate that the combination of intermediate/high zinc intake and high phosphorus intake may lead to a better breast cancer survival.

Additional file 1: Table S1. Pooled imputed values and original values. Table S2a. Mortality status and treatment among the 654 women included in survival analyses. Table S2b. THR��-2 status and treatment modalities among the 654 women included in survival analyses. Table S3. THR��-2 expression, hazard ratios (HRs) with 95% confidence intervals (CI) and Freedman's%, adjusted for a single factor at a time. Table S4. Hazard ratios (HRs) and 95% confidence intervals (CI) for overall mortality per THR��-2 expression, stratified for ER-status and surrogate intrinsic subtype.

The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by the Danish Cancer Society (Kræftens Bekæmpelse) (Denmark), German Cancer Aid (Deutsche Krebshilfe), German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ), Federal Ministry of Education and Research (Bundesministerium fu¨ r Bildung und Forschung, BMBF) (Germany), Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy), Swedish Cancer Society (Cancerfonden), Swedish Research Council (Vetenskapsra° det), County Councils of Ska°ne and Va¨sterbotten (Sweden), Cancer Research UK (14136 to EPIC-Norfolk; C570/ A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk; MR/M012190/1 to EPICOxford) (UK). Infrastructure support for the Department of Epidemiology and Biostatistics at Imperial College London (UK) was provided by the NIHR Imperial Biomedical Research Centre (BRC). The funders had no role in the design and conduct of the study; the collection, analysis and interpretation of the data; or the preparation, review and approval of the manuscript; or in the decision to submit the manuscript for publication., Background: The role of obesity and weight change in breast-cancer development is complex and incompletely understood. We investigated long-term weight change and breast-cancer risk by body mass index (BMI) at age 20 years, menopausal status, hormone replacement therapy (HRT) and hormone-receptor status. Methods: Using data on weight collected at three different time points from women who participated in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, we investigated the association between weight change from age 20 years until middle adulthood and risk of breast cancer. Results: In total, 150 257 women with a median age of 51 years at cohort entry were followed for an average of 14 years (standard deviation¼3.9) during which 6532 breast-cancer cases occurred. Compared with women with stable weight (62.5 kg), long-term weight gain >10 kg was positively associated with postmenopausal breast-cancer risk in women who were lean at age 20 [hazard ratio (HR)¼1.42; 95% confidence interval 1.22–1.65] in ever HRT users (HR¼1.23; 1.04–1.44), in never HRT users (HR¼1.40; 1.16–1.68) and in oestrogen-and-progesterone-receptor-positive (ERþPRþ) breast cancer (HR¼1.46; 1.15–1.85). Conclusion: Long-term weight gain was positively associated with postmenopausal breast cancer in women who were lean at age 20, both in HRT ever users and non-users, and hormone-receptor-positive breast cancer., European Commission (DG-SANCO), International Agency for Research on Cancer, Danish Cancer Society (Kraftens Bekampelse), German Cancer Aid, German Cancer Research Center, Federal Ministry of Education and Research, Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council, Swedish Cancer Society, Swedish Research Council, County Councils of Skane and Vasterbotten, 14136 Cancer Research UK, C570/A16491 EPIC-Norfolk, 1000143 Medical Research Council, Infrastructure support for the Department of Epidemiology and Biostatistics at Imperial College London (UK) was provided by the NIHR Imperial Biomedical Research Centre (BRC)

Additional file 1: Supplementary information. Table S1. Number of metabolites included in each study population; Table S2. Metabolites associated with each anthropometric variable in the replication set; Table S3. Metabolites with the greatest contribution for each metabolic signature; Table S4. Correlations between the metabolic signatures and their corresponding anthropometric measure; Table S5. Metabolites that changed significantly from baseline to follow-up in the Intercept; Table S6. Metabolites significantly associated with weight loss in the Intercept; Table S7. Metabolites significantly associated with weight loss in the Intercept; Figure S1. Overall Rpartial2 and weighted Rpartial2 for each covariate and BMI in the discovery set; Figure S2. Overall Rpartial2 and weighted Rpartial2 for each covariate and WC in the discovery set; Figure S3. Overall Rpartial2 and weighted Rpartial2 for each covariate and WHR in the discovery set; Figure S4. Overall Rpartial2 and weighted Rpartial2 for each covariate and weight loss in the Intercept; Figure S5. Association of colorectal and endometrial cancers with the metabolic signatures further adjusted to C-peptide; Figure S6. Association of colorectal and endometrial cancers with the anthropometric measures of obesity; Figure S7. Smile plot of the associations between metabolites with weight loss in the Intercept.

Additional file 1: Table S1. Population characteristics. Table S2. Spearman rank correlations between dietary intakes of trans fatty acids. Table S3. Food group sources of predominant ruminant and industrial trans fatty acids. Table S4. Associations between dietary intake of trans fatty acids and breast cancer risk according to oestrogen receptor status. Table S5. Associations between dietary intake of trans fatty acids and breast cancer risk according to progesterone receptor status. Table S6. Associations between dietary intake of trans fatty acids and breast cancer risk according to human epidermal growth factor receptor 2 status. Table S7. Associations between dietary intake of trans fatty acids and breast cancer risk according to body mass index group. Table S8. Associations between dietary intake of trans fatty acids and breast cancer risk according to menopausal status. Table S9. Associations between dietary intake of total trans industrial and ruminant fatty acids and breast cancer risk after adjustment for total energy using the residuals method. Table S10. Associations between dietary intake of total trans industrial and ruminant fatty acids and breast cancer risk after mutual adjustment. Table S11. Associations between dietary intake of total trans industrial and ruminant fatty acids and breast cancer risk after adjustment for dietary intakes of saturated fatty acid, monounsaturated fatty acid, and polyunsaturated fatty acid. Table S12. Associations between dietary intake of total trans fatty acids and breast cancer risk adjusted for the World Cancer Research Fund and Mediterranean diet scores. Table S13. P for trend values for the associations between dietary intakes of trans fatty acids and breast cancer risk using the continuous variable and quintile-median approaches. Figure 1. Associations between dietary intake of total trans industrial fatty acids and breast cancer risk by country. Figure 2. Associations between dietary intake of total trans ruminant fatty acids and breast cancer risk by country.

Additional file 3. Distribution of breast cancer treatment and CAP1 tumor-specific expression.

Additional file 2: Figure 1. Post-treatment total cholesterol levels (un-paired samples). Amount of total cholesterol in tumor tissue, after two weeks of treatment with 80 mg atorvastatin daily.