Ross Dickins

Cancer results from an accumulation of genetic mutations that disable the normal regulation of cell growth and survival. In the last decade, large scale cancer genome sequencing of all the major cancer types has identified ~150 genes that promote oncogenesis when mutated. To develop more effective cancer therapies, now the key challenge is to understand how these cancer ‘driver genes’, comprising a similar number of oncogenes and tumour suppressor genes, contribute to tumourigenesis and treatment response.

Our laboratory is interested in understanding tumour suppressor gene function, focusing on several hematopoietic transcription factors recurrently mutated in acute lymphoblastic and myeloid leukemias (ALL and AML). Our general approach uses shRNA-mediated inhibition of these transcription factors to drive leukemogenesis in mice, subsequently assessing the functional consequences of endogenous tumour suppressor restoration in established leukemias in vivo. Using these tools we are gaining fresh insights into how loss of particular transcription factors such as PAX5 and IKAROS contribute to leukemia cell self-renewal and treatment resistance. We are also using leukemias derived from these mouse models to screen for genes critical to leukemia maintenance, which represent potential novel drug targets.

• Awarded Associate Professor and is group leader at The Australian Centre for Blood Diseases, a Monash University department located at the Alfred Hospital in Melbourne
• In 2010, Ross was awarded a $1 million Viertel Foundation Fellowship
• Completed his tertiary education at Melbourne University and his PhD at the Peter MacCallum Cancer Centre
• His groundbreaking work on RNA interference (RNAi) has been published in several top scientific journals including Nature Genetics in 2005 and 2007