Dr Aaron Smith
Dr Vinod Gopalan
UNDERSTANDING CHRONIC CONDITIONS
Topic 13 - Personalised Medicine in Cancer
Dr Aaron Smith began work on the BRN2 transcription factor in 1995 when he explored gene regulation in melanoma as an Honours and then PhD project in the laboratory of A/Prof Richard Sturm at the IMB. A Postdoctoral Fellowship at the University of Cambridge, UK, in 2001 presented an opportunity to gain expertise in Nuclear Receptor biology in metabolic disease. Returning to Australia in 2004, Dr Smith continued working on nuclear receptor function in the context of melanoma and revisited the role of BRN2 in driving phenotype switching in melanoma cells. In 2010 he established an independent research group at the University of Queensland to continue work on gene regulation in melanocyte and melanoma cell function and in 2016 relocated to the QUT, Institute for Health and Biomedical Innovation, Translational Research Institute. In addition to investigating the BRN2-MITF transcriptional axis in melanoma, Dr Smith has research interests in functional analysis of genes and genetic variants associated with nevus count and/or melanoma susceptibility including IRF4, PLA2G6, MTAP and MC1R, and nuclear receptor regulation of DNA repair.
Dr Vinod Gopalan is a Senior Lecturer in Histopathology and an Early Career Researcher in the Schools of Medicine and Medical Science. Dr Gopalan's research focuses on the molecular interactions and its clinical implications in human cancers with particular interests in cancers of the gastrointestinal tract and endocrine organs. Dr Gopalan is one of the Research Leaders in the Cancer Molecular Pathology Laboratory of Menzies Health Institute Queensland where his research investigates many human cancer tissues and blood samples for identifying new markers in Angiogenesis and Cancer Metastasis. Dr Gopalan has published more than 65 peer-reviewed research articles and currently supervises a number of HDR students at Griffith University. He is research active obtaining research and teaching grants and of recent years has received awards and commendations for his achievements.
Dr Aaron Smith - BRN2 - the master regulator of melanoma invasion?
Heterogeneity between two transcription factors in melanoma cells, BRN2 and MITF, has been associated with phenotypic switching between predominantly invasive and proliferative behaviours respectively, thereby allowing adaptation to micro-environmental conditions such as hypoxia, nutrient deprivation and drug treatment. Epigenetic changes, in response to external cues, have been proposed to underpin this process, however the mechanism by which the phenotypic switch occurs is unclear. We have recently identified the NFIB transcription factor as a novel downstream effector of BRN2 function in melanoma cells linked to the migratory and invasive characteristics of these cells. Our data reveal that NFIB has the ability to promote dynamic changes in the chromatin state of melanoma cells to facilitate migration, invasion and metastasis and suggests BRN2 co-ordinates survival responses to environmental cues. Notably, distinct metabolic changes driven by BRN2 offer a potential targeting strategy using novel anticancer agents that de-stabilize mitochondrial function.
Dr Vinod Gopalan - Evolution of tissue-based molecular targets in colorectal cancer pathogenesis
In colorectal cancers, the discovery of K-ras mutations as an indicator of non-responsive anti-epidermal growth factor receptor (EGFR) therapies has revolutionised the use of biomarkers. Our previous research using genetic fingerprinting has revealed many gene candidates with potential biomarker roles in colorectal and other gastrointestinal carcinomas. A potential tumour suppressor candidate, FAM134B and an oncogene named GAEC1 has noted to be significantly involved in regulating colon cancer cell biology by various in-vitro and in-vivo assays. Multiple pieces of evidence from studies strongly suggest the future role of genetic markers or its genetic alterations in cancer cells as a prognostic or predictive marker in colorectal adenocarcinomas.
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