https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 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:12520 Wed 11 Apr 2018 12:41:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27882 Wed 11 Apr 2018 12:08:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32798 Wed 09 Mar 2022 16:01:33 AEDT ]]> 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:48085 Fri 24 Feb 2023 14:56:04 AEDT ]]>