This journey took a logical course along the road of lymphocytes and lymphomas, transcription factors and oncogenes, with some interesting deviations. Graduating as a molecular biologist from the University of Melbourne, my PhD studies at WEHI focussed on common gene rearrangements driving lymphocyte transformation. The culprit was the c-myc proto-oncogene, with both B and T cell tumours suffering activating c-myc mutations, though of different aetiologies. We made the Eµ-myc mouse in 1984 to prove our assertions, and to learn more about the role of myc as an oncogene.  More recently, with P Hodgkin and S Heinzel, we discovered how myc determines cell division capacity, explaining our early observations.

At an exciting moment in 1985, with the first cloning of a Plasmodium falciparum malaria gene, and generous funding, I joined the WEHI malaria group and used new molecular tools to map the parasite genome, describing malaria's chromosomal organisation and its extreme fluidity in vitro and in the field. This is now recognised as a means of the parasite's very the effective immune evasion.

As a postdoctoral fellow in David Baltimore's laboratory at MIT, I witnessed and participated in an amazing variety of discoveries: the cloning of Oct2, NFkB, the E box and Id transcription factors, and the RAG genes. Detailed appreciation of the functions of these proteins required in vivo models, so I generated gene knockouts for Oct2 and RAG1, then continues analyses of the mice in my own laboratory at WEHI.  This set me on my present course of study, with close WEHI colleagues, on the transcriptional regulation of B cells and antibody secreting cells, as well as the T cells and dendritic cells that facilitate an antibody response. Insights gained from this work will be discussed.

Another detour took me slightly off course, and arose as a desire to help Tasmanian investigators (led by Greg Woods) with tools to understand the failed immune response to the lethal, transmissible Tasmanian Devil Facial Tumour Disease (DFTD).  Our findings have helped us work towards a vaccine against this lethal infection (DFT1) and identification of a new isolate (DFT2).