https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30306 Wed 15 Dec 2021 16:09:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35 Wed 11 Apr 2018 16:59:08 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:6849 Wed 11 Apr 2018 16:39:01 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14356 Wed 11 Apr 2018 15:41:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26763 Wed 11 Apr 2018 15:09:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20527 Wed 11 Apr 2018 13:11:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13895 Wed 11 Apr 2018 11:47:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:6851 Wed 11 Apr 2018 10:50:17 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9714 Wed 11 Apr 2018 09:43:06 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27853 T transitions. These mutations are found throughout the melanoma genome, particularly in non-transcribed regions. The global genome repair (GGR) branch of nucleotide excision repair (NER) is responsible for repairing UV-induced DNA damage across non-transcribed and silent regions of the genome. This study aimed to examine the relationship between UVB and GGR in melanoma. DNA repair capacity and relative expression of NER in melanocytes and melanoma cell lines before and after treatment with UVB was quantified. Transcript expression from 196 melanomas was compared to clinical parameters including solar elastosis and whole transcriptome data collected. Melanoma cell lines showed significantly reduced DNA repair when compared to melanocytes, most significantly in the S phase of the cell cycle. Expression of GGR components XPC, DDB1 and DDB2 was significantly lower in melanoma after UVB. In the melanoma tumours, XPC expression correlated with age of diagnosis and low XPC conferred significantly poorer survival. The same trend was seen in the TCGA melanoma dataset. Reduced GGR in melanoma may contribute to the UV mutation spectrum of the melanoma genome and adds further to the growing evidence of the link between UV, NER and melanoma.]]> Wed 02 Mar 2022 14:27:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14315 Sat 24 Mar 2018 08:24:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11525 Sat 24 Mar 2018 08:10:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4898 Sat 24 Mar 2018 07:22:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23143 Sat 24 Mar 2018 07:10:33 AEDT ]]>