https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15687 Wed 11 Apr 2018 11:09:30 AEST ]]> https://ogma.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 ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20038 Sat 24 Mar 2018 07:50:54 AEDT ]]> https://ogma.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 p21^WAF1, 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 ]]>