https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42668 Wed 31 Aug 2022 16:18:23 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53018 Wed 28 Feb 2024 16:09:22 AEDT ]]> 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:54539 Tue 27 Feb 2024 20:41:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46235 Tue 15 Nov 2022 08:51:17 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5341 Sat 24 Mar 2018 07:45:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40395 TP53 SNPs in exon 4 and intron 4 on cancer risk, clinicopathological features and expression of TP53 isoforms. The intron 4 SNPs were significantly over-represented in cohorts of mixed cancers compared to three ethnically matched controls, suggesting they confer increased cancer risk. Further analysis showed that heterozygosity at rs1042522(GC) and either of the two intronic SNPs rs9895829(TC) and rs2909430(AG) confer a 2.34-5.35-fold greater risk of developing cancer. These SNP combinations were found to be associated with shorter patient survival for glioblastoma and prostate cancer. Additionally, these SNPs were associated with tumor-promoting inflammation as evidenced by high levels of infiltrating immune cells and expression of the Δ133TP53 and TP53ß transcripts. We propose that these SNP combinations allow increased expression of the Δ133p53 isoforms to promote the recruitment of immune cells that create an immunosuppressive environment leading to cancer progression.]]> Mon 25 Jul 2022 09:15:39 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41279 Mon 01 Aug 2022 10:24:24 AEST ]]>