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A/Professor Justine Ellis
Dr Justine Ellis is an Australian Research Council Future Fellow and Group Leader of Genes, Environment and Complex Disease at Murdoch Childrens Research Institute.
She trained as a complex disease geneticist at the University of Melbourne, with her early work focusing on adult diseases and traits. Upon moving to Murdoch Childrens in 2007, she established a multidisciplinary program of research called CLARITY - ChiLdhood Arthritis Risk factor Identification sTudY - along with Dr Jane Munro and other Murdoch Childrens and The Royal Children's Hospital colleagues. The design of CLARITY, which collects clinical, epidemiological and environmental data, along with multiple biospecimen types, recognises the multifactorial nature of diseases such as juvenile arthritis. It aims to individually consider the genetic, environmental and epigenetic factors in determining disease, but also importantly, the interplay between them.
With the early support of internal and philanthropic funds, CLARITY has recruited over 1300 participants and has now attracted competitive grant funding from National Health and Medical Research Council and the Australian Research Council.
Dr Ellis also collaborates widely with other research groups working on complex diseases including immune disorders, cardiovascular conditions, and mental health.
- Honorary Senior Research Fellow, Department of Paediatrics, University of Melbourne
- 2012- 2016: Australian Research Council Future Fellowship
Dr Ellis' primary research focus is understanding how genes and environment interact (GxE) to cause complex human disease. Many research programs worldwide are currently tracking down complex disease genes through genome wide association and sequencing based approaches. Some of these research programs focus on environmental influences on disease, but few focus on their interaction, despite the fact that it is very well accepted that complex disease results from genes and environment in combination.
Paediatric immune disorders are an ideal platform upon which to focus GxE research for two reasons. Firstly, the incidence of immune disorders has increased rapidly over the last couple of decades, and this increase is too quick to be able to be explained by population-based changes in genes. Secondly, it is far easier to gather accurate information about environmental exposures prenatally, postnatally, in early life, and at disease onset from children than from adults, since there is a much shorter time-span across which such information needs to be recalled. Dr Ellis' research therefore has a strong focus on paediatric immune disorders, primarily juvenile idiopathic arthritis (JIA), but her group also work closely with researchers interested in type 1 diabetes, food allergy, and crohn's disease. The overall aim of the research is to better understand the underlying determinants of JIA and other disorders, and to advance knowledge more generally as to the role and mechanisms of GxE in complex disease.
- The interaction of genes and environment in JIA
- The role of epigenetics in JIA
- Gene-gene interaction (epistasis) in JIA
- The Paediatric Autoimmune Disease (PAID) collaborative platform at Murdoch Childrens
- ANZCLARITY – A national JIA biobank
RA Chavez Valencia, DJ Martino, R Saffery, JA Ellis. In vitro exposure of human blood mononuclear cells to active vitamin D does not induce substantial change to DNA methylation on a genome scale. Journal of Steroid Biochemistry and Molecular Biology 2014, 141:144-9
JA Ellis, AS Kemp, A-L Ponsonby. Gene-environment interaction in autoimmune diseases. Expert Reviews in Molecular Medicine 2014, 16:e4
JA Ellis, RA Chavez, A Pezic, A-L Ponsonby, JD Akikusa, RC Allen, JE Munro. Independent replication analysis of genetic loci with previous evidence of association with Juvenile Idiopathic Arthritis. Pediatric Rheumatology 2013, 11:12.
JA Ellis, A-L Ponsonby, A Pezic, R Chavez, R Allen, J Akikusa, J Munro. CLARITY: ChiLdhood Arthritis Risk factor Identification sTudY. Paediatric Rheumatology 2012, 10(1):37.
JA Ellis, J Munro, R Chavez, L Gordon, JE Joo, J Akikusa, R Allen, A-L Ponsonby, J Craig, R Saffery. Genome-scale case-control analysis of CD4+ T cell DNA methylation in Juvenile idiopathic Arthritis reveals potential targets involved in disease. Clinical Epigenetics 2012, 4(1):20.
THT Tan, JA. Ellis, JJ. Koplin, MC. Matheson, LC. Gurrin, AJ. Lowe, PE. Martin, TD. Dang, M Wake, MLK Tang, A-L Ponsonby, SC. Dharmage, KJ. Allen, for the HealthNuts Study Investigators. Filaggrin loss-of-function mutations do not predict food allergy over and above the risk of food sensitization amongst infants. Journal of Allergy and Clinical Immunology 2012, 130(5):1211-1213
JA Ellis, AL Ponsonby, A Pezic, E Williamson, J Cochrane, J Dickinson, T Dwyer. APOE genotype and cardio-respiratory fitness interact to determine adiposity in 8 year old children from the Tasmanian Infant Health Survey. PLoS ONE 2011; 6(11): e26679. doi:10.1371/journal.pone.0026679
JE Cobb, N Wong, L Yip, J Martinick, R Bosnich, R Sinclair, J Craig, R Saffery, SB Harrap, JA Ellis. Evidence of increased DNA methylation of the androgen receptor gene in occipital hair follicles from men with androgenetic alopecia. British Journal of Dermatology 2011; 165(1):210-3
JA Ellis, CA Olsson, E Moore, P Greenwood, MOM Van De Ven, GC Patton. A role for the DRD4 exon III VNTR in modifying the association between nicotine dependence and neuroticism. Nicotine and Tobacco Research 2011; 13(2):64-69.
JA Ellis, A-L Ponsonby, J Munro. Possible environmental determinants of Juvenile Idiopathic Arthritis. Rheumatology 2010; 49(3):411-25