https://novaprd-lb.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30306 Wed 15 Dec 2021 16:09:28 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26195 Wed 11 Apr 2018 15:00:42 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:28231 Wed 01 Aug 2018 14:52:20 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:47795 Tue 31 Jan 2023 15:32:49 AEDT ]]> https://novaprd-lb.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://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:54872 Tue 19 Mar 2024 16:38:34 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:52761 Tue 14 Nov 2023 15:30:24 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:47028 Tue 13 Dec 2022 15:55:21 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20561 Tue 10 Oct 2023 08:38:59 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:19379 Thu 29 Aug 2024 11:13:18 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:45124 Thu 27 Oct 2022 10:53:06 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:28088 −6 to P = 7.7 × 10⁻⁵). Only one falls into a haplotype previously associated with other cancer types (rs7705526, in TERT intron 1), and this SNP has been shown to alter TERT promoter activity. One of the novel associations (rs13174814) maps to a second region in the TERT promoter and the other (rs62329728) is in the promoter region of CLPTM1L; neither are correlated with previously reported cancer-associated SNPs. Using TCGA RNASeq data, we found significantly increased expression of both TERT and CLPTM1L in endometrial cancer tissue compared with normal tissue (TERTP = 1.5 × 10⁻¹⁸, CLPTM1LP = 1.5 × 10⁻¹⁹). Our study thus reports a novel endometrial cancer risk locus and expands the spectrum of cancer types associated with genetic variation at 5p15, further highlighting the importance of this region for cancer susceptibility.]]> Thu 08 Aug 2024 15:35:23 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17481 Sat 24 Mar 2018 08:04:10 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17125 −10) that is also associated with risk of prostate cancer and is inversely associated with risk of type 2 diabetes.]]> Sat 24 Mar 2018 08:02:31 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20582 Sat 24 Mar 2018 07:55:36 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26799 Sat 24 Mar 2018 07:36:26 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:48810 Mon 10 Apr 2023 10:28:37 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:44579 Fri 30 Aug 2024 11:04:12 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:46399 313) and questionnaire-based breast cancer risk factors for women of European ancestry, using 72 284 cases and 80 354 controls from the Breast Cancer Association Consortium. Interactions were evaluated using standard logistic regression and a newly developed case-only method for breast cancer risk overall and by estrogen receptor status. After accounting for multiple testing, we did not find evidence that per-standard deviation PRS₃₁₃ odds ratio differed across strata defined by individual risk factors. Goodness-of-fit tests did not reject the assumption of a multiplicative model between PRS₃₁₃ and each risk factor. Variation in projected absolute lifetime risk of breast cancer associated with classical risk factors was greater for women with higher genetic risk (PRS₃₁₃ and family history) and, on average, 17.5% higher in the highest vs lowest deciles of genetic risk. These findings have implications for risk prevention for women at increased risk of breast cancer.]]> Fri 18 Nov 2022 14:15:23 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:47283 Fri 13 Jan 2023 10:24:53 AEDT ]]>