Table2_Antihypertensive medications and risk of colorectal cancer in British Columbia.DOCX

Introduction: There is conflicting evidence for the association between antihypertensive medications and colorectal cancer risk, possibly reflecting methodological limitations of previously conducted studies. Here, we aimed to clarify associations between commonly prescribed antihypertensive medication classes and colorectal cancer risk in a large, retrospective, cohort study.Methods: Using linked administrative data between 1996 and 2017 from British Columbia, we identified a cohort of 1,693,297 men and women who were 50 years of age or older, initially cancer-free and nonusers of antihypertensive medications. Medication use was parameterized as ever use, cumulative duration, and cumulative dose. Cox proportional hazard models were used to estimate hazard ratios (HRs) and associated 95% confidence intervals (95% CIs) for associations of time-varying medication use [angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), beta-blockers (BBs), calcium channel blockers (CCBs), and diuretics] with colorectal cancer risk.Results: There were 28,460 incident cases of colorectal cancer identified over the follow-up period (mean = 12.9 years). When medication use was assessed as ever/never, diuretics were associated with increased risk of colorectal cancer (HR 1.08, 95% CI 1.04–1.12). However, no similar association was observed with cumulative duration or cumulative dose of diuretics. No significant associations between the other four classes of medications and colorectal cancer risk were observed.Conclusion: No compelling evidence of associations between antihypertensive medications and colorectal cancer were observed.</p

Table1_Antihypertensive medications and risk of colorectal cancer in British Columbia.DOCX

Introduction: There is conflicting evidence for the association between antihypertensive medications and colorectal cancer risk, possibly reflecting methodological limitations of previously conducted studies. Here, we aimed to clarify associations between commonly prescribed antihypertensive medication classes and colorectal cancer risk in a large, retrospective, cohort study.Methods: Using linked administrative data between 1996 and 2017 from British Columbia, we identified a cohort of 1,693,297 men and women who were 50 years of age or older, initially cancer-free and nonusers of antihypertensive medications. Medication use was parameterized as ever use, cumulative duration, and cumulative dose. Cox proportional hazard models were used to estimate hazard ratios (HRs) and associated 95% confidence intervals (95% CIs) for associations of time-varying medication use [angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), beta-blockers (BBs), calcium channel blockers (CCBs), and diuretics] with colorectal cancer risk.Results: There were 28,460 incident cases of colorectal cancer identified over the follow-up period (mean = 12.9 years). When medication use was assessed as ever/never, diuretics were associated with increased risk of colorectal cancer (HR 1.08, 95% CI 1.04–1.12). However, no similar association was observed with cumulative duration or cumulative dose of diuretics. No significant associations between the other four classes of medications and colorectal cancer risk were observed.Conclusion: No compelling evidence of associations between antihypertensive medications and colorectal cancer were observed.</p

Supplementary Figure 1 from Lifetime Physical Activity and the Risk of Non-Hodgkin Lymphoma

Physical activity questionnaire used in a case-control study of non-Hodgkin lymphoma conducted in British Columbia, Canada, 2000-2004.</p

Supplementary Table 2 from Lifetime Physical Activity and the Risk of Non-Hodgkin Lymphoma

Distribution of total, moderate-intensity and vigorous-intensity physical activity performed in specific age-periods by cases and controls in a case-control study conducted in British Columbia, Canada, 2000-2004.</p

Supplementary Table 1 from Lifetime Physical Activity and the Risk of Non-Hodgkin Lymphoma

Distribution of lifetime total, moderate-intensity and vigorous-intensity physical activity by sex and non-Hodgkin lymphoma subtype in a case-control study conducted in British Columbia, Canada, 2000-2004.</p

Supplementary Figure 2 from Lifetime Physical Activity and the Risk of Non-Hodgkin Lymphoma

Directed acyclic graph used to select covariates in the analysis of the association between physical activity and the risk of non-Hodgkin lymphoma in a case-control study conducted in British Columbia, Canada, 2000-2004.</p

Supplementary Table 3 from Lifetime Physical Activity and the Risk of Non-Hodgkin Lymphoma

Associations between total, moderate-intensity and vigorous-intensity physical activity performed in specific age-periods and the risk of non-Hodgkin lymphoma in a case-control study conducted in British Columbia, Canada, 2000-2004.</p

Supplementary data from Young Adult and Usual Adult Body Mass Index and Multiple Myeloma Risk: A Pooled Analysis in the International Multiple Myeloma Consortium (IMMC)

Table S1. Characteristics of the case-control studies included in the International Multiple Myeloma Consortium (IMMC) Lifestyle Factors Pooling Project (LFPP). Table S2. Usual adult BMI and pooled relative risk of multiple myeloma in population-based case-control studies within category of selected demographic risk factors. Table S3. Usual adult BMI and pooled relative risk of multiple myeloma in hospital-based case-control studies within category of selected demographic risk factors. Table S4. Pooled relative risk of multiple myeloma by category of weight and height: overall and by study design and interview type.</p

Data_Sheet_1_Genetically Determined Height and Risk of Non-hodgkin Lymphoma.docx

Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00–1.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01–1.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes.</p

Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukaemia

Several chronic lymphocytic leukaemia (CLL) susceptibility loci have been reported; however, much of the heritable risk remains unidentified. Here we perform a meta-analysis of six genome-wide association studies, imputed using a merged reference panel of 1,000 Genomes and UK10K data, totalling 6,200 cases and 17,598 controls after replication. We identify nine risk loci at 1p36.11 (rs34676223, P=5.04 × 10−13), 1q42.13 (rs41271473, P=1.06 × 10−10), 4q24 (rs71597109, P=1.37 × 10−10), 4q35.1 (rs57214277, P=3.69 × 10−8), 6p21.31 (rs3800461, P=1.97 × 10−8), 11q23.2 (rs61904987, P=2.64 × 10−11), 18q21.1 (rs1036935, P=3.27 × 10−8), 19p13.3 (rs7254272, P=4.67 × 10−8) and 22q13.33 (rs140522, P=2.70 × 10−9). These new and established risk loci map to areas of active chromatin and show an over-representation of transcription factor binding for the key determinants of B-cell development and immune response