My research focuses blood disorders primarily affecting children, caused by inherited gene changes (mutations). The only available treatment for such disorders is bone marrow transplant, but it is often difficult to find suitable donors, and even when we can, risks such transplant rejection can result in life-threatening complications and treatment failure.
Genetic blood disorders have a serious effect on the quality of life and life-expectancy of children. My goal is to change that by ‘editing’ the genes that ultimately cause these disorders.
I aim to restore normal function to a person’s own bone marrow cells by repairing the gene mutation that drives disease – making transplant unnecessary. I have developed several tools to repair ‘faulty’ DNA sequences, which are now being tested in the lab.
My work has also established genome editing (CRISPR/Cas9) as a new discipline for SVI, which is now being used in the Genome Stability laboratory and across other projects and laboratory groups.
My research interests: genome editing (CRISPR/Cas9), DNA damage repair, gene therapy
Key achievements
2022 Winner of the Inaugural Captain Courageous Fellowship
2021 SVI Rising Star Award
2019-2021 SVI Rising Star Fellowship from the Janko Inge Foundation
2016 Best Gene Therapy Paper Award from the Australasian Gene and Cell Therapy Society
Selected publications
Howden SE, McColl B, Glaser A, Vadolas J, Petrou S, Little MH, Elefanty AG, Stanley EG. (2016). A Cas9 Variant for Efficient Generation of Indel-Free Knockin or Gene-Corrected Human Pluripotent Stem Cells. Stem Cell Reports. 7(3):508-517
Glaser A, McColl B, Vadolas J. (2016). GFP to BFP Conversion: A Versatile Assay for the Quantification of CRISPR/Cas9-mediated Genome Editing. Mol Ther Nucleic Acids. 5(7):e334
Glaser A, McColl B, Vadolas J. (2015). The therapeutic potential of genome editing for β-thalassemia. F1000 Faculty Rev-1431
Kalb ML, Glaser A, Stary G, Koszik F, Stingl G. (2012). TRAIL(+) human plasmacytoid dendritic cells kill tumor cells in vitro: mechanisms of imiquimod- and IFN-α-mediated antitumor reactivity. J Immunol. 188(4):1583-91