ORCID Profile
0000-0003-3919-7261
Current Organisation
Garvan Institute of Medical Research
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Elsevier BV
Date: 09-2010
Publisher: Royal Society of Chemistry (RSC)
Date: 2019
DOI: 10.1039/C9RP00057G
Abstract: Despite the advancements in the production and accessibility of videos and animations, a gap exists between their potential for science teaching and their actual use in the classroom. The aim of this study was to develop and evaluate an approach to boost chemistry and biology teachers’ Technological Pedagogical Content Knowledge (TPACK) and their confidence regarding the use of videos and animations in class, which are required for their effective implementation. Twelve experienced high-school chemistry and biology teachers participated in a professional development workshop including biochemistry and technological–pedagogical lectures along with video-editing instruction and practice. Teachers were provided with digital videos including high-resolution scientifically based animations and were encouraged to edit them based on their pedagogical experience and the needs of their class. We investigated how the workshop affected teachers' TPACK-confidence and TPACK. TPACK-confidence was assessed by pre- and post-workshop questionnaires and open-ended feedback questionnaires. TPACK was assessed by analyses of the edited digital videos and pedagogical considerations submitted by the teachers. It was found that teachers' TPACK-confidence was significantly higher following the workshop. There was also a development in the teachers' TPACK. They were able to recommend to use digital videos in a variety of classroom situations based on the technological pedagogical knowledge ( e.g. , as an opening to a new topic) and their TPACK ( e.g. , to visualize complex biochemical processes). We also found a development in their video-editing skills and their knowledge of how to use this technology effectively in biochemistry lessons. Results indicate that training teachers in using technological tools while providing them with relevant Content Knowledge and TPACK, and relying on their pre-existing Pedagogical Content Knowledge may assist them develop their TPACK and TPACK-confidence. This may promote the effective use of videos and animations in biochemistry teaching.
Publisher: Elsevier BV
Date: 08-2009
DOI: 10.1016/J.YGYNO.2009.04.031
Abstract: The urokinase plasminogen activator (uPA) system has been implicated in progression and poor prognosis in epithelial ovarian cancer (EOC) patients. The present study investigated the distribution of uPA and its receptor (uPAR) in EOC cell lines, primary and metastatic tumors, and the relationship between uPA/uPAR and matrix metalloproteinase (MMP) expression using immunohistochemistry. We also studied the association between uPA/uPAR expression and clinical and pathological parameters including disease progression free survival (PFS). The expression of uPA/uPAR was examined on paraffin-embedded tissue sections from primary EOC (n=100), and matched metastatic lesions (n=30) of untreated patients, normal ovarian tissues (n=20) as well as 8 primary and metastatic EOC cell lines by immunohistochemistry. Co-immunolabeling of uPA and MMP-1, -2, -9 or MT1-MMP was examined using confocal microscopy. The expression of uPA/uPAR was found in most primary (92% and 88% positive, respectively), metastatic ovarian tumors (93% and 90% positive, respectively), and all of examined EOC cell lines. The majority of specimens showed moderate to strong immunostaining of tumor and stromal cells for primary specimens, this was significantly associated with tumor stage, grade and time to relapse (P<0.01). Overexpression of uPA/uPAR was found to be associated with an unfavorable prognosis with significantly reduced median disease PFS of 16 vs. 33 months for uPA (P<0.001), and 15 vs. 28 months for uPAR (P<0.001). Co-localization of uPA with MMP-1, -2, -9 or MT1-MMP was also seen in primary tumors and metastatic lesions. The expression of uPA/uPAR was associated with EOC progression. uPA/uPAR are useful markers for EOC prognosis and could be promising therapeutic targets for treating incurable, recurrent EOC.
Publisher: American Association for Cancer Research (AACR)
Date: 2011
DOI: 10.1158/1055-9965.EPI-10-0719
Abstract: Background: Previously, we showed that gene suppression commonly occurs across chromosome 2q14.2 in colorectal cancer, through a process of long-range epigenetic silencing (LRES), involving a combination of DNA methylation and repressive histone modifications. We now investigate whether LRES also occurs in prostate cancer across this 4-Mb region and whether differential DNA methylation of 2q14.2 genes could provide a regional panel of prostate cancer biomarkers. Methods: We used highly sensitive DNA methylation headloop PCR assays that can detect 10 to 25 pg of methylated DNA with a specificity of at least 1:1,000, and chromatin immunoprecipitation assays to investigate regional epigenetic remodeling across 2q14.2 in prostate cancer, in a cohort of 195 primary prostate tumors and 90 matched normal controls. Results: Prostate cancer cells exhibit concordant deacetylation and methylation of histone H3 Lysine 9 (H3K9Ac and H3K9me2, respectively), and localized DNA hypermethylation of EN1, SCTR, and INHBB and corresponding loss of H3K27me3. EN1 and SCTR were frequently methylated (65% and 53%, respectively), whereas INHBB was less frequently methylated. Conclusions: Consistent with LRES in colorectal cancer, we found regional epigenetic remodeling across 2q14.2 in prostate cancer. Concordant methylation of EN1 and SCTR was able to differentiate cancer from normal (P & 0.0001) and improved the diagnostic specificity of GSTP1 methylation for prostate cancer detection by 26%. Impact: For the first time we show that DNA methylation of EN1 and SCTR promoters provide potential novel biomarkers for prostate cancer detection and in combination with GSTP1 methylation can add increased specificity and sensitivity to improve diagnostic potential. Cancer Epidemiol Biomarkers Prev 20(1) 148–59. ©2011 AACR.
Publisher: Springer Science and Business Media LLC
Date: 18-03-2008
Publisher: Springer Science and Business Media LLC
Date: 06-08-2012
DOI: 10.1038/ONC.2012.300
Abstract: Deregulation of microRNA (miRNA) expression can have a critical role in carcinogenesis. Here we show in prostate cancer that miRNA-205 (miR-205) transcription is commonly repressed and the MIR-205 locus is hypermethylated. LOC642587, the MIR-205 host gene of unknown function, is also concordantly inactivated. We show that miR-205 targets mediator 1 (MED1, also called TRAP220 and PPARBP) for transcriptional silencing in normal prostate cells, leading to reduction in MED1 mRNA levels, and in total and active phospho-MED1 protein. Overexpression of miR-205 in prostate cancer cells negatively affects cell viability, consistent with a tumor suppressor function. We found that hypermethylation of the MIR-205 locus was strongly related with a decrease in miR-205 expression and an increase in MED1 expression in primary tumor s les (n=14), when compared with matched normal prostate (n=7). An expanded patient cohort (tumor n=149, matched normal n=30) also showed significant MIR-205 DNA methylation in tumors compared with normal, and MIR-205 hypermethylation is significantly associated with biochemical recurrence (hazard ratio=2.005, 95% confidence interval (1.109, 3.625), P=0.02), in patients with low preoperative prostate specific antigen. In summary, these results suggest that miR-205 is an epigenetically regulated tumor suppressor that targets MED1 and may provide a potential biomarker in prostate cancer management.
Publisher: Elsevier BV
Date: 06-2022
DOI: 10.1016/J.TIG.2022.03.003
Abstract: Molecular animations can be beneficial as teaching tools for genomics education however, barriers to their effective implementation remain. This article proposes informed design guidelines from the perspective of the animator that may assist others to effectively communicate scientific concepts to their respective audiences and communities.
Publisher: ACM
Date: 14-11-2019
Publisher: Elsevier BV
Date: 05-2012
DOI: 10.1016/J.CANLET.2011.12.003
Abstract: To identify epigenetic-based biomarkers for diagnosis of ovarian cancer we performed MeDIP-Chip in A2780 and CaOV3 ovarian cancer cell lines. Validation by Sequenom massARRAY methylation analysis confirmed a panel of six gene promoters (ARMCX1, ICAM4, LOC134466, PEG3, PYCARD & SGNE1) where hypermethylation discriminated 27 serous ovarian cancer clinical s les versus 12 normal ovarian surface epithelial cells (OSE) (ROC of 0.98). Notably, CpG sites across the transcription start site of a potential long-intergenic non-coding RNA (lincRNA) gene (LOC134466), was shown to be hypermethylated in 81% of serous EOC and could differentiate tumours from OSE (p<0.05). We propose that this potential biomarker panel holds great promise as a diagnostic test for high-grade (Type II) serous ovarian cancer.
Publisher: Cold Spring Harbor Laboratory
Date: 25-07-2011
Abstract: Histone H2A.Z (H2A.Z) is an evolutionarily conserved H2A variant implicated in the regulation of gene expression however, its role in transcriptional deregulation in cancer remains poorly understood. Using genome-wide studies, we investigated the role of promoter-associated H2A.Z and acetylated H2A.Z (acH2A.Z) in gene deregulation and its relationship with DNA methylation and H3K27me3 in prostate cancer. Our results reconcile the conflicting reports of positive and negative roles for histone H2A.Z and gene expression states. We find that H2A.Z is enriched in a bimodal distribution at nucleosomes, surrounding the transcription start sites (TSSs) of both active and poised gene promoters. In addition, H2A.Z spreads across the entire promoter of inactive genes in a deacetylated state. In contrast, acH2A.Z is only localized at the TSSs of active genes. Gene deregulation in cancer is also associated with a reorganization of acH2A.Z and H2A.Z nucleosome occupancy across the promoter region and TSS of genes. Notably, in cancer cells we find that a gain of acH2A.Z at the TSS occurs with an overall decrease of H2A.Z levels, in concert with oncogene activation. Furthermore, deacetylation of H2A.Z at TSSs is increased with silencing of tumor suppressor genes. We also demonstrate that acH2A.Z anti-correlates with promoter H3K27me3 and DNA methylation. We show for the first time, that acetylation of H2A.Z is a key modification associated with gene activity in normal cells and epigenetic gene deregulation in tumorigenesis.
Publisher: IEEE
Date: 2017
Publisher: Springer Science and Business Media LLC
Date: 27-05-2008
Publisher: Portland Press Ltd.
Date: 25-02-2009
DOI: 10.1042/BJ20082234
Abstract: DUSPs (dual-specificity phosphatases) are a heterogeneous group of protein phosphatases that can dephosphorylate both phosphotyrosine and phosphoserine hosphothreonine residues within the one substrate. DUSPs have been implicated as major modulators of critical signalling pathways that are dysregulated in various diseases. DUSPs can be ided into six subgroups on the basis of sequence similarity that include slingshots, PRLs (phosphatases of regenerating liver), Cdc14 phosphatases (Cdc is cell ision cycle), PTENs (phosphatase and tensin homologues deleted on chromosome 10), myotubularins, MKPs (mitogen-activated protein kinase phosphatases) and atypical DUSPs. Of these subgroups, a great deal of research has focused on the characterization of the MKPs. As their name suggests, MKPs dephosphorylate MAPK (mitogen-activated protein kinase) proteins ERK (extracellular-signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 with specificity distinct from that of in idual MKP proteins. Atypical DUSPs are mostly of low-molecular-mass and lack the N-terminal CH2 (Cdc25 homology 2) domain common to MKPs. The discovery of most atypical DUSPs has occurred in the last 6 years, which has initiated a large amount of interest in their role and regulation. In the past, atypical DUSPs have generally been grouped together with the MKPs and characterized for their role in MAPK signalling cascades. Indeed, some have been shown to dephosphorylate MAPKs. The current literature hints at the potential of the atypical DUSPs as important signalling regulators, but is crowded with conflicting reports. The present review provides an overview of the DUSP family before focusing on atypical DUSPs, emerging as a group of proteins with vastly erse substrate specificity and function.
Publisher: MyJove Corporation
Date: 21-10-2011
DOI: 10.3791/3170
No related grants have been discovered for Kate Patterson.