https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24073 -11). SNP rs727479 was also among those most strongly associated with circulating E₂ concentrations in 2767 post-menopausal controls (P=7.4x10^-8). The observed endometrial cancer odds ratio per rs727479 A-allele (1.15, CI=1.11-1.21) is compatible with that predicted by the observed effect on E₂ concentrations (1.09, CI=1.03-1.21), consistent with the hypothesis that endometrial cancer risk is driven by E₂. From 28 candidate-causal SNPs, 12 co-located with three putative gene-regulatory elements and their risk alleles associated with higher CYP19A1 expression in bioinformatical analyses. For both phenotypes, the associations with rs727479 were stronger among women with a higher BMI (P_interaction=0.034 and 0.066 respectively), suggesting a biologically plausible gene-environment interaction.]]> Wed 19 Apr 2023 16:42:45 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30306 Wed 15 Dec 2021 16:09:28 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27984 Wed 15 Dec 2021 16:06:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35727 Wed 14 Jun 2023 12:38:16 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6849 Wed 11 Apr 2018 16:39:01 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26763 Wed 11 Apr 2018 15:09:54 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26195 Wed 11 Apr 2018 15:00:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6851 Wed 11 Apr 2018 10:50:17 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4378 A, causes overexpression and supports uncontrollable cellular growth. This polymorphism has been associated with an increased risk of developing many cancers, including endometrial cancer. Methods: The 870 G>A polymorphisms (rs605965) in the cyclin D1 gene was genotyped in an Australian endometrial cancer case-control population including 191 cases and 291 controls using real-time PCR analysis. Genotype analysis was performed using chi-squared (χ²) statistics and odds ratios were calculated using unconditional logistic regression, adjusting for potential endometrial cancer risk factors. Results: Women homozygous for the variant cyclin D1 870 AA genotype showed a trend for an increased risk of developing endometrial cancer compared to those with the wild-type GG genotype, however this result was not statistically significant (OR 1.692 95% CI (0.939-3.049), p = 0.080). Moreover, the 870 G>A polymorphism was significantly associated with family history of colorectal cancer. Endometrial cancer patients with the homozygous variant AA genotype had a higher frequency of family members with colorectal cancer in comparison to endometrial cancer patients with the GG and combination of GG and GA genotypes (GG versus AA; OR 2.951, 95% CI (1.026-8.491), p = 0.045, and GG+GA versus AA; OR 2.265, 95% CI (1.048-4.894), p = 0.038, respectively). Conclusion: These results suggest that the cyclin D1 870 G>A polymorphism is possibly involved in the development of endometrial cancer. A more complex relationship was observed between this polymorphism and familial colorectal cancer.]]> Wed 11 Apr 2018 10:44:26 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:9714 Wed 11 Apr 2018 09:43:06 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49053 Wed 03 May 2023 15:47:22 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30018 Tue 20 Sep 2022 14:49:52 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:47028 Tue 13 Dec 2022 15:55:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20561 Tue 10 Oct 2023 08:38:59 AEDT ]]> https://ogma.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.]]> Tue 10 Oct 2023 08:38:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26776 Thu 11 Apr 2019 13:18:13 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:9354 Sat 24 Mar 2018 08:36:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7107 Sat 24 Mar 2018 08:34:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17481 Sat 24 Mar 2018 08:04:10 AEDT ]]> https://ogma.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://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26799 Sat 24 Mar 2018 07:36:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24769 Pathology.]]> Sat 24 Mar 2018 07:14:07 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48810 Mon 10 Apr 2023 10:28:37 AEST ]]>