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Additional file 2. CAP1 protein expression grouped according to immunohistochemical staining. (A) Distribution over CAP1 scoring, (B) distribution over CAP1 scoring after grouping, (C) breast cancer-specific survival (BCSS) of all five different CAP1 scoring, (D) overall survival (OS) of all five different CAP1 scoring. Patients at risk and number of events (NoE) are shown.

Additional file 1. Validation of CAP1 antibody specificity and functional validity using a genetic approach of siRNA-mediated target knockdown. (A) Graphs displaying relative CAP1 mRNA expression in T47D and MDA-MB-231 cells following siRNA-induced CAP1 knockdown or non-silencing control (B) Quantification of relative CAP1 protein levels and Western immunoblotting showing reduction of protein bands detected by Abcam ab133655 at the expected molecular size (52 kDa) after CAP1 silencing, (C) Immunocytochemistry images visualizing CAP1 protein abundance in cell microarray of T47D and MDA-MB-231 in CAP1 knockdown or control cells. Error bars show standard error of means from three independent experiments.

Additional file 3: Figure 2. Proliferation of MCF-7 cells treated with atorvastatin. The proliferation of MCF-7 cells treated with 5, 10, 20, 50 and 100 μM atorvastatin for 72 h relative to untreated control. The MCF-7 cell proliferation decreased in a concentration-dependent manner.

Additional file 4. Overall survival (OS) according to CAP1 expression, stratified for (A) body fat percentage (BF%), (B) body mass index (BMI), (C) waist circumference, and (D) waist-hip ratio (WHR). Patients at risk, number of events (NoE), LogRank trend test and adjusted hazard ratios (HRs) with 95% CI comparing low CAP1 expression to high CAP1 expression are shown. HR adjusted for age at diagnosis (continuous), tumor size (> 20 mm, yes/no) and any axillary lymph node involvement (yes/no).

Additional file 5: Figure 4. LDLR expression in MCF-7 cells after atorvastatin treatment. (A) Atorvastatin moderately increased LDLR protein expression in MCF-7 cells treated with atorvastatin (10 μM) after 48 h of treatment, but no statistical difference was found (student’s T-test). Values are expressed as the geometric mean ± 95% confidence interval of the geometric mean of three independent experiments. (B) LDLR relative abundance was measured using Western blot analysis normalized to GAPDH.

Additional file 4: Figure 3. Total cholesterol levels in MCF-7 cells after treatment with atorvastatin. No statistical difference was found between the total cholesterol levels in MCF-7 cells after treatment with 10 μM atorvastatin for 24, 48 and 72 h, respectively, compared to MCF-7 cells cultured in absence of atorvastatin (2-way ANOVA). Values are expressed as the mean ± standard deviation of three independent experiments.

Insulin‐like growth factor (IGF)‐I has cancer promoting activities. However, the hypothesis that circulating IGF‐I concentration is related to risk of lymphoma overall or its subtypes has not been examined prospectively. IGF‐I concentration was measured in pre‐diagnostic plasma samples from a nested case–control study of 1,072 cases of lymphoid malignancies and 1,072 individually matched controls from the European Prospective Investigation into Cancer and Nutrition. Odds ratios (ORs) and confidence intervals (CIs) for lymphoma were calculated using conditional logistic regression. IGF‐I concentration was not associated with overall lymphoma risk (multivariable‐adjusted OR for highest versus lowest third = 0.77 [95% CI = 0.57–1.03], p trend = 0.06). There was no statistical evidence of heterogeneity in this association with IGF‐I by sex, age at blood collection, time between blood collection and diagnosis, age at diagnosis, or body mass index (p heterogeneity for all ≥ 0.05). There were no associations between IGF‐I concentration and risk for specific BCL subtypes, T‐cell lymphoma or Hodgkin lymphoma, although number of cases were small. In this European population, IGF‐I concentration was not associated with risk of overall lymphoma. This study provides the first prospective evidence on circulating IGF‐I concentrations and risk of lymphoma. Further prospective data are required to examine associations of IGF‐I concentrations with lymphoma subtypes., What's new? Insulin‐like growth factor I does not appear to influence lymphoma risk, according to new results. IGF‐I can promote some cancers, but there hasn't been a prospective epidemiological study examining the link between IGF‐I concentration and lymphoma risk. To uncover a link, these authors arranged a NESTED case–control study with participants from the European Prospective Investigation into Cancer and Nutrition (EPIC). They tested for IGF‐I in pre‐diagnosis samples and found no association between the factor and overall lymphoma risk, nor with any subtype, although the number of cases was small for each subtype, and further studies are necessary.

Insulin-like growth factor (IGF)-I has cancer promoting activities. However, the hypothesis that circulating IGF-I concentration is related to risk of lymphoma overall or its subtypes has not been examined prospectively. IGF-I concentration was measured in pre-diagnostic plasma samples from a nested case-control study of 1,072 cases of lymphoid malignancies and 1,072 individually matched controls from the European Prospective Investigation into Cancer and Nutrition. Odds ratios (ORs) and confidence intervals (CIs) for lymphoma were calculated using conditional logistic regression. IGF-I concentration was not associated with overall lymphoma risk (multivariable-adjusted OR for highest versus lowest third = 0.77 [95% CI = 0.57-1.03], p(trend) = 0.06). There was no statistical evidence of heterogeneity in this association with IGF-I by sex, age at blood collection, time between blood collection and diagnosis, age at diagnosis, or body mass index (pheterogeneity for all >= 0.05). There were no associations between IGF-I concentration and risk for specific BCL subtypes, T-cell lymphoma or Hodgkin lymphoma, although number of cases were small. In this European population, IGF-I concentration was not associated with risk of overall lymphoma. This study provides the first prospective evidence on circulating IGF-I concentrations and risk of lymphoma. Further What’s new? Insulin-like growth factor I does not appear to influence lymphoma risk, according to new results. IGF-I can promote some cancers, but there hasn’t been a prospective epidemiological study examining the link between IGF-I concentration and lymphoma risk. To uncover a link, these authors arranged a NESTED case-control study with participants from the European Prospective Investigation into Cancer and Nutrition (EPIC). They tested for IGF-I in pre-diagnosis samples and found no association between the factor and overall lymphoma risk, nor with any subtype, although the number of cases was small for each subtype, and further studies are necessary.