Joe Trapani is Head of the Cancer Immunology Program at Peter MacCallum Cancer Centre Melbourne, and until recently was Peter Mac’s Executive Director Cancer Research (2009-2018) and Inaugural Head of the Sir Peter MacCallum Department of Oncology at The University of Melbourne (2012-18). In 2018, he was appointed Director of the new Centre for Cancer Immunotherapy for Peter Mac and the VCCC partners.
Joe’s research interests include the immunopathology of viral and auto-immune diseases, apoptosis induction by cytotoxic lymphocytes and cancer immunotherapy. He has authored > 310 research papers, reviews and book chapters (>24K cites, H-index 82). Joe Trapani has been a member of the Executive (Board) of the Cancer Council Victoria since 2007, and Chaired its Medical and Scientific Committee since 2013. Joe participates in many other peer-review bodies for State and Federal governments, and in academia and industry.
Joe Trapani received his medical degree in 1977 and his PhD in 1985 from UoM. He completed physician training in rheumatology (FRACP 1985) and received his PhD in the immunogenetics of B27-related arthropathy.
Joe became interested in how the immune system defends against viruses and cancer while a post-doc at Sloan-Kettering Cancer Institute, New York. Here, he discovered a number of the genes and proteins used by killer lymphocytes to eliminate virus-infected cells. He found that one protein (perforin) forms pores in the target cell and provides access for other proteins (granzymes) to enter and trigger cell death by apoptosis. Joe’s subsequent work provided strong evidence in support of Burnet’s controversial but crucial hypothesis of ‘cancer immune surveillance’. He has been inducted into two learned societies: FAHMS (2015) and FAA (2018).
With his colleagues, Professor Trapani has since 1995 been devising CAR T therapy – using gene engineering approaches to harness the power of killer lymphocytes as adoptive immunotherapy for various cancers. Joe’s team has further identified a rare group of children with inherited defects of perforin and shown that they more frequently develop leukaemia.