https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36541 Wed 23 Feb 2022 16:01:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30784 Wed 11 Apr 2018 13:21:37 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30999 Wed 09 Feb 2022 15:59:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29580 BRCA1/2 mutations have a genetic predisposition for developing OC, but not all of these women develop the disease. Epidemiological findings show that lifestyle factors such as contraceptive use and pregnancy, a progesterone dominant state, decrease the risk of getting OC. How ovarian hormones modify the risk of OC is currently unclear. Our study identifies activated Wnt signalling to be a marker for precursor lesions of OC and successfully develops a mouse model that mimics the earliest events in pathogenesis of OC by constitutively activating ßcatenin. Using this model and human OC cells, we show that oestrogen promotes and progesterone suppresses the growth of OC cells.]]> Wed 09 Feb 2022 15:54:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43015 Wed 09 Aug 2023 12:26:25 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50850 Wed 09 Aug 2023 09:39:07 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53981 Thu 25 Jan 2024 12:57:12 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41255 Sat 30 Jul 2022 13:01:25 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44716 Fri 21 Oct 2022 09:04:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53114 Fri 17 Nov 2023 11:41:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35929 MED12 alterations in 39 of 65 fibroids (60%) from 14 patients. Using isobaric tagged-based quantitative mass spectrometry on three selected patients (n = 9 fibroids), we observed a common set of upregulated ( > 1.5-fold) and downregulated ( < 0.66-fold) proteins in small, medium, and large fibroid samples of annotated MED12 status. These two sets of upregulated and downregulated proteins were the same in all patients, regardless of variations in fibroid size and MED12 status. We then focused on one of the significant upregulated ECM proteins and confirmed the differential expression of periostin using western blotting and immunohistochemical analysis. Our study defined the proteome of uterine fibroids and identified that increased ECM protein expression, in particular periostin, is a hallmark of uterine fibroids regardless of MED12 mutation status. This study sets the foundation for further investigations to analyze the mechanisms regulating ECM overexpression and the functional role of upregulated ECM proteins in leiomyogenesis.]]> Fri 17 Jan 2020 11:35:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45565 1.5-fold) with a confidence corresponding to false discovery rate (FDR) <1% in small-, medium-, and large-sized fibroid samples regardless of MED12 mutation status. The TNC was validated on additional patient samples using Western blotting (WB) and immunohistochemistry (IHC) and confirmed significant overexpression of this protein in fibroids compared to matched ANM. Proteomic analyses have identified the increased ECM protein expression, TNC, as a hallmark of uterine fibroids regardless of MED12 mutations. Further functional studies focusing on the upregulated ECM proteins in leiomyogenesis will lead to the identification of novel ECM drug targets for fibroid treatment.]]> Fri 04 Nov 2022 14:44:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51354 Fri 01 Sep 2023 13:44:28 AEST ]]>