https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22647 Wed 22 May 2019 14:51:24 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6281 Wed 11 Apr 2018 16:43:21 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:15053 Wed 11 Apr 2018 13:24:44 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20808 Wed 11 Apr 2018 12:16:47 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:26534 Wed 06 Apr 2022 14:04:50 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:154 g and Nt540c>t, which have been detected in other populations. To establish if they are associated with an increased malignant melanoma (MM) risk we did an association study based on genotyping 471 patients with MM and 1,2 10 random control subjects from the same Polish population. We found a significantly increased frequency of the A148T variant among patients with MM (7.0%) in comparison with the general population (2.9%). The incidence of the A148T variant remained greater in both unselected and familial melanoma subgroups. A statistically significant positive association was seen for unselected MM (odds ratio, 2.529; P = 0.0003), especially in patients diagnosed under 50 years of age (odds ratio, 3.4; P = 0.0002). The A148T carrier population (heterozygous G/A alleles) was more likely to have a relative with malignancy compared with the noncarrier population (57% versus 36%, respectively; P = 0.03). Further examination of the CDKN2A promoter sequence done in 20 melanoma patients with the A148T change (heterozygous G/A alleles) and 20 patients with MM without this alteration identified it was in linkage disequilibrium with a polymorphism in the promoter region at position P-493. We found no statistically significant overrepresentation of the Nt500c>g and the Nt540c>t polymorphisms in the Polish melanoma population. In conclusion, the A148T variant of the CDKN2A gene seems to be associated with an increased risk of development of MM. Additional studies are required to confirm whether this particular change is associated with increased risk of other nonmelanoma malignancies.]]> Thu 25 Jul 2013 09:09:40 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43306 Thu 15 Sep 2022 13:54:25 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6850 Sat 24 Mar 2018 10:23:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8339 T and 1298 A>C, that alter the function of the encoded protein have been the focus of many studies on CRC risk outside the context of an inherited predisposition to disease. In this report, a total of 417 HNPCC participants were genotyped for the 677 C>T and 1298 A>C SNPs to determine whether there exists an association with the age of disease onset of CRC. Genotyping of both SNPs was performed by TaqMan assay technology. Associations in disease risk were further investigated using Kaplan–Meier survival analysis and Cox hazard regression. The average ages of disease diagnosis were found to be different between individuals harbouring either one of the MTHFR polymorphisms. Both Kaplan–Meier and Cox hazard regression analyses revealed a more complex relationship between the two polymorphisms and the age of CRC onset. The Kaplan–Meier survival analysis revealed that compound heterozygotes for the two SNPs developed CRC 10 years later compared with those carrying only wild-type alleles.]]> Sat 24 Mar 2018 08:39:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7033 Sat 24 Mar 2018 08:37:51 AEDT ]]> 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:7800 Sat 24 Mar 2018 08:33:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12486 Sat 24 Mar 2018 08:15:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4898 Sat 24 Mar 2018 07:22:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34107 T CC genotype has been previously linked to FD and TT genotype to antidepressant response in depression. The ss genotype of the 5-HTT LPR variant of the serotonin transporter gene (SLC6A4) has been linked to selective serotonin reuptake inhibitor (SSRI) response. We aimed to examine whether GNβ3 825C>T and 5-HTT LPR polymorphisms result in differential treatment effects in FD patients receiving antidepressant therapy. Methods: Participants were randomized to receive placebo, 50 mg AMI, or 10 mg escitalopram (ESC). The primary end point was adequate relief for ≥5 weeks of the last 10 weeks. Genotyping of GNβ3 825C>T and 5-HTT LPR was performed utilizing PCR-based methods. Results: GNβ3 825C>T and 5-HTT LPR genotype data were available for 256 (88%) and 246 (84%) patients, respectively. Both polymorphisms were in Hardy-Weinberg equilibrium. In tests for differential treatment, neither 5-HTT LPR nor GNβ3 825C>T genotype influenced response to therapy (P=0.89 and P=0.54, respectively). Although there was a tendency for a more favorable response to ESC in the SS/LS genotype compared to the LL genotype groups (40% vs. 31% reporting adequate relief of FD symptoms) among those in the ESC treatment arm, this was not significant (P=0.43). Conclusions: GNβ3 825C>T and 5-HTT LPR genetic variants do not alter treatment response to tricyclic and SSRI antidepressants in FD.]]> Fri 08 Feb 2019 10:43:58 AEDT ]]>