Understanding immune dysfunction in acute myeloid leukemia

Research Opportunity
PhD, Honours, Master of Biomedical Science
Biochemistry and Molecular Biology
Bio21 Molecular Science and Biotechnology Institute
Primary Supervisor Email Number Webpage
Dr Justine Mintern jmintern@unimelb.edu.au 83442976 Personal web page
Co-supervisor Email Number Webpage
Professor Jose Villadangos j.villadangos@unimelb.edu.au

Project Details

The growth factor receptor tyrosine kinase flt3 is the most frequently mutated gene in acute myeloid leukemia (AML). Flt3 is expressed by immune cells and promotes their function and survival. Patients with flt3 mutations have poorer prognosis and more aggressive disease.

In this project, we will examine molecular mechanisms that regulate flt3 receptor in healthy settings and in a model of AML. We will use microscopy, immunoprecipitation and flow cytometry to examine how the mutated flt3 receptor, compared to wild type receptor, is trafficked inside immune cells. These studies will incorporate the use of CRISPR/Cas9 to delete genes identified in patient studies that are implicated in flt3 function. In addition, we will examine how mutant flt3 impacts the ability of immune cells to elicit effective immunity.

Faculty Research Themes

Cancer, Infection and Immunology

School Research Themes

Cancer in Biomedicine, Cell Signalling, Molecular Mechanisms of Disease, Infection & Immunity

Research Opportunities

PhD, Honours, Master of Biomedical Science
Students who are interested in joining this project will need to consider their elegibility as well as other requirements before contacting the supervisor of this research

Graduate Research application

Honours application

Key Contact

For further information about this research, please contact a supervisor.


Biochemistry and Molecular Biology

Research Group / Unit / Centre

Mintern laboratory: Vaccine biology

Research Node

Bio21 Molecular Science and Biotechnology Institute

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