https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53342 13,000 adult and pediatric tumor samples across 38 distinct cancer cohorts from The Cancer Genome Atlas and The Therapeutically Applicable Research to Generate Effective Treatments data sets. The differences between canonical miRNAs and the wider miRNAome in terms of expression, clustering, dysregulation, and prognostic standpoint were investigated. The combination of canonical miRNAs and modified miRNAs boosted the quality of clustering results, outlining unique clinicopathologic features among cohorts. Certain modified miRNAs showed opposite expression from their canonical counterparts in cancer, potentially impacting their targets and function. Finally, a shifted and edited miRNA isoform was experimentally validated to directly bind and suppress a unique target. These findings outline the importance of going beyond the well-established paradigm of one mature miRNA per miRNA arm to elucidate novel mechanisms related to cancer progression.]]> Wed 22 Nov 2023 10:18:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5046 Wed 11 Apr 2018 10:25:08 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29356 Tff1) gene and the tamoxifen-inducible Cre recombinase (CreERT2)–coding sequence. The resulting Tg(Tff1-CreERT2) mice were crossed with mice harboring conditional oncogenic mutations in Kras or Braf. The administration of tamoxifen to the resulting adult Tg(Tff1-CreERT2);Kras^LSL-G12D/+ and Tg(Tff1-CreERT2);Braf^LSL-V600E/+ mice resulted in gastric metaplasia, inflammation, and adenoma development, characterized by excessive STAT3 activity. To assess the contribution of STAT3 to the spontaneously developing gastric adenomas in gp130^F/F mice, which carry a knockin mutation in the Il6 signal transducer (Il6st), we generated Tg(Tff1-CreERT2);Stat3^fl/fl;gp130^F/F mice that also harbor a conditional Stat3 knockout allele and found that tamoxifen administration conferred a significant reduction in their tumor burden. Conversely, excessive Kras activity in Tg(Tff1-CreERT2);Kras^LSL-G12D/+;gp130^F/F mice promoted more extensive gastric inflammation, metaplastic transformation, and tumorigenesis than observed in Tg(Tff1-CreERT2);Kras^LSL-G12D/+ mice. Collectively, our findings demonstrate that advanced gastric tumorigenesis requires oncogenic KRAS or BRAF in concert with aberrant STAT3 activation in epithelial precursor cells of the glandular stomach, providing a new conditional model of gastric cancer in which to investigate candidate therapeutic targets and treatment strategies.]]> Wed 09 Mar 2022 16:03:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32181 Wed 09 Mar 2022 15:58:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35745 chromosome 9 open reading frame 3 gene that was transcriptionally activated by p53. Similarly, the host gene of miRNA-455-3p, collagen alpha-1 (XXVII) chain, was also a p53 transcriptional target. Collectively, our results identify miRNA-27b-3p and miRNA-455-3p as important regulators of cancer cell quiescence in response to p53 and suggest that manipulating miRNA-27b-3p and miRNA-455-3p may constitute novel therapeutic avenues for improving outcomes of cancer treatment. Significance: Two novel p53-responsive microRNAs whose distinct mechanisms of action both stabilize p27 to promote cell quiescence and may serve as therapeutic avenues for improving outcomes of cancer treatment.]]> Thu 28 Oct 2021 12:36:09 AEDT ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33114 Thu 24 Mar 2022 11:29:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1921 50 years of age was significantly elevated compared with the control population (odds ratio, 2.23; P = 0.0046). The results indicate that NOD2 may be a predisposing factor to colorectal cancer characterized by an older average age of disease onset in persons who do not harbor any other genetic predisposition to disease.]]> Sat 24 Mar 2018 08:33:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1093 Sat 24 Mar 2018 08:31:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1606 Sat 24 Mar 2018 08:30:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11381 Sat 24 Mar 2018 08:11:51 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:19635 Sat 24 Mar 2018 08:01:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5319 Sat 24 Mar 2018 07:45:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:130 Sat 24 Mar 2018 07:43:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:333 Sat 24 Mar 2018 07:42:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28919 Sat 24 Mar 2018 07:25:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53140 Fri 17 Nov 2023 11:42:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49407 Fri 12 May 2023 14:55:16 AEST ]]>