https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29799 Wed 15 Dec 2021 16:09:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26066 Thu 20 Aug 2020 09:19:59 AEST ]]> 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 ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27570 Sat 24 Mar 2018 07:23:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41710 HNF4A and GATA6, switch metabolic profiles from classical (pancreatic) to predominantly squamous, with glycogen synthase kinase 3 beta (GSK3β) a key regulator of glycolysis. Pharmacological inhibition of GSK3β results in selective sensitivity in the squamous subtype; however, a subset of these squamous patient-derived cell lines (PDCLs) acquires rapid drug tolerance. Using chromatin accessibility maps, we demonstrate that the squamous subtype can be further classified using chromatin accessibility to predict responsiveness and tolerance to GSK3β inhibitors. Our findings demonstrate that distinct patterns of chromatin accessibility can be used to identify patient subgroups that are indistinguishable by gene expression profiles, highlighting the utility of chromatin-based biomarkers for patient selection in the treatment of PDAC.]]> Fri 12 Aug 2022 08:35:16 AEST ]]>