https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Hypermutation in pancreatic cancer https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34276 MLH1 and MSH2. Defining mutation load in individual pancreatic cancers and the optimal assay for patient selection may inform clinical trial design for immunotherapy in pancreatic cancer.]]> Thu 13 Jan 2022 10:31:35 AEDT ]]> Clinical and pathologic features of familial pancreatic cancer https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18742 2 years) was associated with poor survival in both groups.Conclusions: FPC represents 9% of PC, and the risk of malignancy in kindred does not appear to be confined to the pancreas. Patients with FPC have more precursor lesions and include fewer active smokers, but other clinicopathologic factors and outcome are similar to those in patients with SPC. Furthermore, some FPC kindreds may exhibit anticipation. A better understanding of the clinical features of PC will facilitate efforts to uncover novel susceptibility genes and the development of early detection strategies.]]> Sat 24 Mar 2018 08:02:49 AEDT ]]> Histomolecular phenotypes and outcome in adenocarcinoma of the ampulla of Vater https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20038 Sat 24 Mar 2018 07:50:54 AEDT ]]> The epigenetic agents suberoylanilide hydroxamic acid and 5-AZA-2' deoxycytidine decrease cell proliferation, induce cell death and delay the growth of MiaPaCa2 pancreatic cancer cells in vivo https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27522 in vitro and in vivo models. Treatment with HDACi [suberoylanilide hydroxamic acid (SAHA)] and DNMTi [5-AZA-2' deoxycytidine (5-AZA-dc)] decreased cell proliferation in MiaPaCa2 cells, and SAHA treatment, with or without 5-AZA-dc, resulted in higher cell death and lower DNA synthesis compared to 5-AZA-dc alone and controls (DMSO). Further, combination treatment with SAHA and 5-AZA-dc significantly increased expression of p21WAF1, leading to G1 arrest. Treatment with epigenetic agents delayed tumour growth in vivo, but did not decrease growth of established pancreatic tumours. In conclusion, these data demonstrate a potential role for epigenetic modifier drugs for the management of PC, specifically in the chemoprevention of PC, in combination with other chemotherapeutic agents.]]> Sat 24 Mar 2018 07:28:54 AEDT ]]> Whole genomes redefine the mutational landscape of pancreatic cancer https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27570 Sat 24 Mar 2018 07:23:30 AEDT ]]> Precision oncology in surgery: patient selection for operable pancreatic cancer https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46225 Fri 09 Dec 2022 14:48:55 AEDT ]]>