Dr Jim Vadolas received his PhD from the University of Melbourne, Department of Microbiology and Immunology, where he developed novel adjuvant technologies designed to enhance immune responses to vaccines. In 1999, Dr Vadolas undertook postdoctoral studies at the Murdoch Children’s Research Institute, where he acquired expertise in genetic and molecular techniques utilising bacterial artificial chromosome (BACs) and homologous recombination systems.
In 2005, Dr Vadolas became group leader of the Cell and Gene Therapy group, primarily interested in the development of novel therapeutic strategies for β-thalassaemia and related β‑haemoglobinopathies. There, he established several unique cell-based assay systems and clinically relevant animal models of β‑thalassaemia. These innovations enabled investigations that provided important insights into the epigenetic mechanism(s) involved in globin gene regulation throughout development and disease. A major aspect of his research is the development and evaluation of genetic-based approaches involving lentiviral gene therapy and genome editing.
More recently, Dr Vadolas’ expertise in β‑haemoglobinopathies enabled his group to establish a new research program investigating how iron overload contributes to aberrant innate immune responses in β‑thalassaemia. Dysregulation of iron homeostasis in inherited or acquired anaemias may tip the immunoregulatory balance to allow increased growth rates of infectious organisms and cancer cells, and therefore complicate the clinical management of acute and chronic diseases.
Dr Vadolas is a research group leader at Hudson Institute and co-heads the Immunohaematology research group with Dr George Grigoriadis. Dr Vadolas is the current Vice President of the Australasian Gene and Cell Therapy Society, and has served as Committee Member and Vice President of the Thalassaemia and Sickle Cell Society of Australia from 2005-2017.
Thiengtavor C, Siriworadetkun S, Paiboonsukwong K, Fucharoen S, Pattanapanyasat K, Vadolas J, Svasti S, Chaichompoo P (2019) Increased ferritin levels in β-thalassaemia/HbE are associated with reduced CXCR2 expression and neutrophil migration. Br J Haematol.
Siwaponanan P, Siegers J, Gazahli M, Ng N, McColl B, Svasti S, Fucharoen S, Wijburg O, Vadolas J (2017) Reduced PU.1 expression underlies aberrant neutrophil maturation and function in β‑thalassemia. Blood 129:3087-3099.
Lee W, McColl B, Maksimovic J, Vadolas J (2017) Epigenetic interplay at the β-globin locus. Biochim Biophys Acta Gene Regul Mech 1860:393-404.
McColl B, Vadolas J (2016) Animal models of β-hemoglobinopathies: utility and limitations. J Blood Med 7:263-274.
Kraidith K, Svasti S, Teerapornpuntakit J, Vadolas J, Chaimana R, Lapmanee S, Suntornsaratoon P, Krishnamra N, Fucharoen S, Charoenphandhu N (2016) Hepcidin and 1,25(OH)2D3 effectively restore Ca2+ transport in beta-thalassemic mice: reciprocal phenomenon of Fe2+ and Ca2+ absorption. Am J Physiol Endocrinol Metab 311:E214-223.
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:e334.
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 7:508-517.
Wienert B, Funnell AP, Norton LJ, Pearson RC, Wilkinson-White LE, Lester K, Vadolas J, Porteus MH, Matthews JM, Quinlan KG, Crossley M (2015) Editing the genome to introduce a beneficial naturally occurring mutation associated with increased fetal globin. Nat Commun 6:7085.
McColl B, Kao B, Lourthai P, Chan K, Wardan H, Roosjen M, Delagneau O, Gearing LJ, Blewitt ME, Svasti S, Fucharoen S, Vadolas J (2014) An in vivo model for analysis of developmental erythropoiesis and globin gene regulation. FASEB J 28:2306-2317.
Roosjen M, McColl B, Kao B, Gearing LJ, Blewitt ME, Vadolas J (2014) Transcriptional regulators Myb and BCL11A interplay with DNA methyltransferase 1 in developmental silencing of embryonic and fetal β-like globin genes. FASEB J 28:1610-1620.