Congratulations to our recently completed PhD students, Michelle Flynn and Ethan Oxley

Ethan Oxley

Michelle Flynn

Congratulations to our recently completed PhD students, Michelle Flynn and Ethan Oxley, whose PhD awards were conferred 21 April 2021. We wish them well for their future scientific careers.

 Ms Michelle Flynn's thesis is titled "Investigating the Role of Neutrophil Glucose Metabolism in Inflammation and Diabetes-Associated Myelopoiesis and Atherosclerosis". Michelle was supervised by Professor Andrew Murphy and Dr Man Kit Sam Lee, Baker Heart and Diabetes Institute.

Michelle says, "Neutrophils contribute to the pathogenesis of a number of inflammatory diseases, often linked to either global metabolic disturbances and/or changes to immune cell metabolism. Here, we explored the role of neutrophil glucose metabolism in promoting inflammation in diabetes. We modelled this in the context of transient and intermittent hyperglycaemia prevalent in patients with seemingly well-controlled glucose levels, to explore the contribution to atherosclerosis. We also reveal novel functions for potential regulators of neutrophil glucose metabolism: GLUT-6 (uptake) and hexokinase-3 (1-step metabolism) in mediating diabetes and inflammation associated neutrophil production and function."

Mr Ethan Oxley's thesis is titled, "PU.1 and maturational plasticity in acute myeloid leukaemia". Ethan was supervised by Associate Professor Ross Dickins and Associate Professor Matt McCormack, Australian Centre for Blood Diseases.

Ethan says, "Acute myeloid leukaemia (AML) is a haematological malignancy often framed in the context of a hierarchical leukaemia stem cell model, where only a small proportion of immature leukaemia cells maintain the entire tumour bulk. In this project, we demonstrate that mature and non-leukaemogenic AML cells can reacquire leukaemia-initiating activity and promote disease progression through de-differentiation. Furthermore, extensive mechanistic and transcriptomic analysis revealed that this maturational plasticity was largely dependent on the myeloid transcription factor PU.1, a protein frequently disrupted in AML. These results prompt new interpretations of intratumoural phenotypic heterogeneity in AML, and may reveal novel avenues of disease relapse."