Ross Dickins

Assoc Professor

Accepting PhD Students

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Personal profile


Ross is a laboratory head at the Australian Centre for Blood Diseases, a Monash University department at the Alfred Hospital. As a postdoctoral scientist in New York he helped develop RNA interference technology allowing reversible inhibition of endogenous gene expression in cultured cells and in mice. His laboratory now uses these tools to investigate hematopoiesis and leukemia, focusing on genes recurrently mutated in acute myeloid leukemia (AML). Of particular interest is understanding how mutations affecting transcription factors impose the maturation block in acute leukemia, and novel approaches to trigger leukemia differentiation and prevent relapse. His lab also studies how myeloid lineage antigen-presenting cells regulate T cell costimulation in autoimmunity and cancer.

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Supervision interests

Novel immunosuppressive mechanisms of CTLA4 and CTLA4-Ig therapies

Self-reactive T cells cause many autoimmune diseases, and can also trigger serious autoimmune side-effects in cancer patients undergoing immunotherapy. T cell activation normally occurs upon interaction with antigen-presenting cells (APCs) expressing surface ligands for the T cell receptor and the costimulatory receptor CD28. Surface CTLA4 expressed by activated T cells or regulatory T cells (Tregs) dampens T cell activation and restrains autoimmunity by outcompeting CD28 for their shared costimulatory ligands CD80 and CD86 expressed on the APC surface. Recombinant homodimeric CTLA4-Ig fusion proteins also bind CD80 and CD86 to prevent T cell costimulation, and CTLA4-Ig therapies including abatacept are widely used clinically for autoimmune disease and organ transplant rejection.

Acute myeloid leukaemia differentiation therapy response and relapse

Acute myeloid leukaemia (AML) is caused by accumulated oncogenic mutations in white blood cell progenitors that lock them into an immature self-renewing state. Approximately 1000 Australians are diagnosed with AML each year, but less than one third will survive beyond 5 years. Most AML patients are treated with cytotoxic chemotherapy that kills immature leukaemia cells but also normal cells, with dose-limiting side effects and high relapse rates. In contrast to chemotherapy, AML differentiation therapy triggers leukaemia maturation leading to the subsequent clearance of mature leukaemia-derived cells. In principle AML differentiation therapy is preferable to chemotherapy because it avoids widespread genotoxic cell death. Instead, triggering leukaemia maturation engages highly efficient clearance mechanisms that normally turn over 100 billion mature myeloid cells (predominantly neutrophils) daily. Several new AML differentiation therapies have recently entered the clinic. Unfortunately, while many initially yield robust clinical responses, relapse remains almost inevitable. Surprisingly little is known about the phenotype and fate of mature leukaemia-derived cells in patients on differentiation therapy, because these cells are often indistinguishable from normal mature myeloid cells. The cellular origin of AML relapse following differentiation therapy also remains poorly understood, and preventing relapse remains a major clinical challenge.

Expertise related to UN Sustainable Development Goals

In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This person’s work contributes towards the following SDG(s):

  • SDG 3 - Good Health and Well-being

Research area keywords

  • Acute myeloid leukaemia
  • Acute lymphoblastic leukaemia
  • Tumour suppressor genes
  • Transcription factors
  • Differentiation therapy

Collaborations and top research areas from the last five years

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