16 research outputs found
Incremental cost and QALYs of precision and age-based screening compared with no screening.
Results based on 10,000 simulations. The solid lines describe the incremental costs incurred and QALYs gained of precision screening versus no screening, whilst the dashed lines represent the incremental costs and QALYs of age-based versus no screening. QALY, quality-adjusted life-year.</p
Outcomes of age-based and precision screening compared with no screening.
Outcomes of age-based and precision screening compared with no screening.</p
Overdiagnosed cases and prostate cancer deaths prevented with precision screening as compared to age-based screening.
Results based on 10,000 simulations.</p
Supplementary Figure 1 from A Cross-Cancer Genetic Association Analysis of the DNA Repair and DNA Damage Signaling Pathways for Lung, Ovary, Prostate, Breast, and Colorectal Cancer
Supplemental Figure 1: Manhattan plot, illustrating p-values from 60,297 SNP associations, generated from each of the 10 studies used in the meta-analysis. Statistical significance threshold is denoted by the red line (p = 5.09 x 10-6).</p
Supplemental Tables 1-5 and Legend to Supplemental Figure 1 from A Cross-Cancer Genetic Association Analysis of the DNA Repair and DNA Damage Signaling Pathways for Lung, Ovary, Prostate, Breast, and Colorectal Cancer
Supplemental Table 1: Detailed characteristics of studies included in the ASSET meta-analysis of DNA damage repair and signaling genes. Supplemental Table 2: DNA repair gene, region, and final SNP selection data, using human reference genome assembly, GRCh38. Supplemental Table 3: List of all DNA repair genes and DNA repair pathways included in this study. Supplemental Table 4: Statistical associations (p-values) for cancer risk versus genetic variation within DNA repair pathways. Sensitivity analysis of Table 3, with RAD51B, MSH5, and BRCA2 gene removed from analysis. Statistically significant values are in bold (p < 0.05). Supplemental Table 5: Statistical associations (p-values) for cancer risk versus genetic variation within DNA repair pathways. Sensitivity analysis of Table 3, with 6 genes removed from the analysis -- all genes containing loci with individual SNP associations of p < 1 x 10-4. Statistically significant values are in bold (p < 0.05).</p
Additional file 1 of Risk-reducing salpingo-oophorectomy, natural menopause, and breast cancer risk: an international prospective cohort of BRCA1 and BRCA2 mutation carriers
Additional file 1 : Table S1. Studies and samples included in the prospective cohort of BRCA1 and BRCA2 mutation carriers. Table S2. Distributions of dates of breast cancer diagnosis, DNA test and start of follow-up in the prospective cohort. Table S3. Characteristics of reported Risk-Reducing Salpingo-oophorectomy. Table S4. Characteristics of cohort of BRCA1 and BRCA2 mutation carriers. Table S5. Association between RRSO and breast cancer by menopausal status. Table S6. Association between RRSO and breast cancer (sensitivity analysis with RRSO status changing at the age at the questionnaire with information on RRSO status changes (all studies except HEBON)). Table S7. Association between RRSO and breast cancer (sensitivity analysis dropping individuals with missing information at baseline). Table S8. Association between RRSO and breast cancer among BRCA1 and BRCA2 mutation carriers (sensitivity analysis excluding women with RRSO before baseline). Table S9. Association between family history of breast cancer and family history of ovarian cancer and RRSO uptake. Table S10. Association between parity, age at first birth, and body mass index and RRSO uptake. Table S11. Association between RRSO and breast cancer adjusting for Body Mass Index, family history of breast cancer, family history of ovarian cancer, parity and age at first birth. Table S12. Hormone replacement therapy use among women in the cohort. Table S13. Association between RRSO and breast cancer among women not exposed to hormone replacement therapy. Table S14. Association between RRSO and breast cancer (excluding kConFab/BCFR). Table S15. Association between natural menopause and breast cancer (censoring at RRSO). Ethics Committee Approval
Associations between selected SNPs from 9p22.2 and ovarian cancer in <i>BRCA1</i>, <i>BRCA2</i> and combined analysis of <i>BRCA1/2</i> mutation carriers.
Associations between selected SNPs from 9p22.2 and ovarian cancer in BRCA1, BRCA2 and combined analysis of BRCA1/2 mutation carriers.</p
Additional file 2: of Male breast cancer in BRCA1 and BRCA2 mutation carriers: pathology data from the Consortium of Investigators of Modifiers of BRCA1/2
List of local ethics committees that granted approval for the access and use of the data in present study. (DOCX 23 kb
Conditional associations for <i>BRCA1</i> and <i>BRCA2</i> top SNPs.
<p><b>The table shows the HR estimate. 95% CI and p-value for the conditional analysis adjusting for the lead SNP in the univariate analysis for <i>BRCA1</i> (left hand side) or <i>BRCA2</i> mutation carriers (right had side).</b> SNPs correspond to: rs10124837, the strongest associated in <i>BRCA1</i>; rs62543583, the strongest associated in <i>BRCA2</i> mutation carriers; rs7046326, the strongest associated in <i>BRCA1/2</i> meta-analysis; rs3814113, was the strongest associated variant in the initial GWAS analysis. “HR”, hazard ratio; “CI”, confidence interval.</p
