Prof Ricky Johnstone: Identification of epigenetic and genetic regulators of anti-tumor immunity
Location:Centenary Institute, Camperdown
Prof Ricky Johnstone, Executive Director Cancer Research, Peter Mac Callum Cancer Centre
Altered expression, function or localisation of epigenetic enzymes and/or their partner proteins can play a crucial role in cancer onset and progression. The effects of BET bromodomain inhibitors (BETi) on tumor cell growth and survival have been well documented. However, BETi also have immunomodulatory properties that could be important for anti-tumor responses and could be harnessed to enhance the activities of other anti-cancer agents. I will present data showing that BETi can affect anti-tumor immune response through effects on both the target tumor cells and on immune cells. These properties are important for the anti-tumor effects of BETi and can be exploited to devise novel combination regimes involving epigenetic regulators and immune modulators.
Professor Ricky Johnstone received his PhD from the University of Melbourne in 1993 and after a postdoc at Harvard Medical School returned to Melbourne to establish the Gene Regulation Laboratory at the Peter MacCallum Cancer Centre in 2000.
Professor Johnstone is the Executive Director Cancer Research at the Peter MacCallum Cancer Centre overseeing ~700 staff and students and plays a key role in strategic decision making across the organisation. He has published more than 230 peer-reviewed papers, was awarded an NHMRC Senior Principal Research Fellowship in 2015 and in 2011 was promoted to Full Professor in the Department of Pathology at the University of Melbourne.
Prof Johnstone is a cancer researcher who has utilized genetic mouse models of hemopoietic malignancies and solid tumors to understand the epigenetic changes that underpin tumor onset and progression and to develop new therapies that target epigenetic and transcriptional regulatory proteins.
Prof Johnstone has recently discovered how epigenetic based-agents can engage the host immune system to drive prolonged therapeutic responses.