Andrew’s role within the Kinghorn Centre for Clinical Genomics (KCCG) is to facilitate the appliance and integration of genomics into both medical research and clinical practice in Australia. His role encompasses science communication and stakeholder engagement, through to the procurement and management of genomic projects.
Andrew’s background is primarily in scientific research and project management in both academia and industry. After completion of his PhD at Cardiff University (UK), and holding research positions at both Novartis (Horsham, UK) and RSR Biotech (Cardiff, UK), Andrew joined the Garvan Institute of Medical Research in 2010, to continue his research into the molecular mechanisms that underpin acquired endocrine resistance in breast cancer. In 5 years as a post-doc at the Garvan, Andrew contributed to 12 publications, 6 as first author, and was involved in the management of a collaborative, multi-million dollar National Breast Cancer Foundation program grant, focused on the identification of molecular biomarkers for breast cancer diagnosis, prognosis and predictors of drug response using next generation sequencing technologies. During this time, he developed an enthusiasm for genomic technologies and their role in the future of scientific research and healthcare. He subsequently joined the KCCG in March 2015, and is excited to be involved in this new genomic frontier in health and medicine.
In the NewsHow some breast cancers become resistant to hormone therapy - Jul 15, 2015
New hope for hormone resistant breast cancer - Jul 23, 2013
Awards and Honours
2014 – Best Oral Presentation – Garvan Post-Doc Symposium
2004 – BSc (Hons), Pharmacology, University of Bath – UK
Stone, A. et al. DNA methylation of oestrogen-regulated enhancers defines endocrine sensitivity in breast cancer. Nature communications 6 (2015).
Stirzaker, C. et al. Methylome sequencing in triple-negative breast cancer reveals distinct methylation clusters with prognostic value. Nature communications 6 (2015).
Locke, W. J. et al. Coordinated epigenetic remodelling of transcriptional networks occurs during early breast carcinogenesis. Clinical epigenetics 7, 1-15 (2015).
Stone, A. & Musgrove, E. A. Endocrine therapy: defining the path of least resistance. Breast Cancer Research 14, R48 (2014).
Stone, A., Valdes-Mora, F. & Clark, S. J. Exploring and exploiting the aberrant DNA methylation profile of endocrine-resistant breast cancer. Epigenomics 5, 595-598 (2013).
Stone, A. et al. BCL-2 hypermethylation is a potential biomarker of sensitivity to antimitotic chemotherapy in endocrine-resistant breast cancer. Molecular cancer therapeutics 12, 1874-1885 (2013).
Browne, B. C. et al. Global characterization of signalling networks associated with tamoxifen resistance in breast cancer. FEBS Journal 280, 5237-5257 (2013).
Stone, A. et al. Tamoxifen-induced epigenetic silencing of oestrogen-regulated genes in anti-hormone resistant breast cancer. PloS one 7, e40466 (2012).
Stone, A., Sutherland, R. L. & Musgrove, E. A. Inhibitors of cell cycle kinases: recent advances and future prospects as cancer therapeutics. Critical Reviews™ in Oncogenesis 17 (2012).
Kalyuga, M. et al. ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer. PLoS Biol 10, e1001461 (2012).
Caldon, C. E. et al. Cyclin E2 overexpression is associated with endocrine resistance but not insensitivity to CDK2 inhibition in human breast cancer cells. Molecular cancer therapeutics 11, 1488-1499 (2012).
Musgrove, E. A., Caldon, C. E., Barraclough, J., Stone, A. & Sutherland, R. L. Cyclin D as a therapeutic target in cancer. Nature Reviews Cancer 11, 558-572 (2011).