https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29559 G and c.3113G > A, CHEK2 c.349A > G, c.538C > T, c.715G > A, c.1036C > T, c.1312G > T, and c.1343T > G and ATM c.7271T > G. We assessed associations with breast cancer risk (42 671 cases and 42 164 controls), as well as prostate (22 301 cases and 22 320 controls) and ovarian (14 542 cases and 23 491 controls) cancer risk, for each variant. Results: For European women, strong evidence of association with breast cancer risk was observed for PALB2 c.1592delT OR 3.44 (95% CI 1.39 to 8.52, p=7.1×10-5), PALB2 c.3113G > A OR 4.21 (95% CI 1.84 to 9.60, p=6.9×10-8) and ATM c.7271T > G OR 11.0 (95% CI 1.42 to 85.7, p=0.0012). We also found evidence of association with breast cancer risk for three variants in CHEK2, c.349A > G OR 2.26 (95% CI 1.29 to 3.95), c.1036C > T OR 5.06 (95% CI 1.09 to 23.5) and c.538C > T OR 1.33 (95% CI 1.05 to 1.67) (p=0.017). Evidence for prostate cancer risk was observed for CHEK2 c.1343T > G OR 3.03 (95% CI 1.53 to 6.03, p=0.0006) for African men and CHEK2 c.1312G > T OR 2.21 (95% CI 1.06 to 4.63, p=0.030) for European men. No evidence of association with ovarian cancer was found for any of these variants. Conclusions This report adds to accumulating evidence that at least some variants in these genes are associated with an increased risk of breast cancer that is clinically important.]]> Wed 09 Feb 2022 15:56:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47795 Tue 31 Jan 2023 15:32:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50431 Tue 25 Jul 2023 19:01:27 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46467 P < 5 × 10⁻⁸) were identified as instrumental variables, and assessed using genome-wide association study data from the Endometrial Cancer Association Consortium (12 906 cases and 108 979 controls) and the Global Lipids Genetic Consortium (n = 188 578). Mendelian randomization analyses found genetically raised LDL cholesterol levels to be associated with lower risks of endometrial cancer of all histologies combined, and of endometrioid and non-endometrioid subtypes. Conversely, higher genetically predicted HDL cholesterol levels were associated with increased risk of non-endometrioid endometrial cancer. After accounting for the potential confounding role of obesity (as measured by genetic variants associated with body mass index), the association between genetically predicted increased LDL cholesterol levels and lower endometrial cancer risk remained significant, especially for non-endometrioid endometrial cancer. There was no evidence to support a role for triglycerides in endometrial cancer development. Our study supports a role for LDL and HDL cholesterol in the development of non-endometrioid endometrial cancer. Further studies are required to understand the mechanisms underlying these findings.]]> Tue 19 Sep 2023 15:34:26 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54872 Tue 19 Mar 2024 16:38:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45124 Thu 27 Oct 2022 10:53:06 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46914 Thu 08 Dec 2022 08:47:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47283 Fri 13 Jan 2023 10:24:53 AEDT ]]>