Rate My Professor Matthew McCormack

Matthew McCormack is an Adjunct Associate Professor (Research) at the Australian Centre for Blood Diseases in the Faculty of Medicine, Nursing and Health Sciences at Monash University. As a cell biologist, he possesses extensive experience in induced pluripotent stem cell (iPSC) derivation and their utilization for cell therapy, regenerative medicine, and cell-based immuno-oncology. His research encompasses transcriptional and epigenetic control of stem cells, oncogene cooperation, and genetic evolution in the context of cancer biology. McCormack leads the iPSC-based Cell Therapy group, a collaboration between Monash University and iCamuno Biotherapeutics, focusing on advancing methods for iPSC reprogramming and genome editing. This work aims to develop therapies for cellular rejuvenation through partial reprogramming, as well as iPSC-derived treatments for immuno-oncology and regenerative applications targeting conditions such as Parkinson’s disease, ophthalmic diseases, osteoarthritis, and various cancers.

McCormack's career trajectory includes postdoctoral fellowships at the MRC Laboratory of Molecular Biology in Cambridge, United Kingdom, and the Royal Melbourne Hospital. He has held Laboratory Head positions at the Walter and Eliza Hall Institute of Medical Research and Monash University. In 2022, he assumed the role of Senior Director at iCamuno Biotherapeutics, a biotechnology startup dedicated to iPSC-based cell therapies. His contributions to the field are evidenced by over 40 publications in prestigious journals such as Science, New England Journal of Medicine, Journal of Clinical Investigation, Blood, and Journal of Experimental Medicine. Notable works include 'The Lmo2 oncogene initiates leukemia in mice by inducing thymocyte self-renewal' (Science, 2010), 'Activation of the T-cell oncogene LMO2 following gene therapy for X-linked Severe Combined Immunodeficiency' (New England Journal of Medicine, 2004), 'Overexpression of Lmo2 initiates T-lymphoblastic leukemia via impaired thymocyte competition' (Journal of Experimental Medicine, 2023), 'Acute myeloid leukemia requires Hhex to enable PRC2-mediated epigenetic repression of Cdkn2a' (Genes & Development, 2016), and 'T-ALL can evolve to oncogene independence' (Leukemia, 2021). He has also received funding from the National Health and Medical Research Council for projects investigating the multistep pathogenesis of T-cell leukemia and the role of homeobox genes in acute myeloid leukemia.