Following the award of her PhD in 2008 (Swinburne University), Dr Walton joined the Growth Factor Therapeutics Laboratory at Prince Henry's Institute of Medical Research (Clayton), alongside Dr Craig Harrison and A/Prof David Robertson. In 2016, she moved to Monash University where she now co-heads the Growth Factor Therapeutics Laboratory in the Department of Physiology. Her research interest is transforming growth factor ‐β (TGF‐β) biology. TGF‐β proteins regulate cell growth and are frequently altered in chronic human diseases including cancers and infertility. Kelly’s initial findings defined how TGF‐β proteins are assembled in humans (Journal of Biological Chemistry, 2009. 284:9311‐9320; Journal of Biological Chemistry, 2010. 285:17029‐37) which enabled the generation of a specific TGF‐β based therapeutics (Endocrinology, 152:3758‐68). The new class of TGF‐β protein therapeutics have exciting potential in the treatment of metabolic wasting associated with cancer and aging.

Physiological Consequences of the Loss of Inhibin Activity -

Gonadal-derived inhibin A and inhibin B are essential factors in mammalian reproduction, negatively regulating pituitary production of follicle stimulating hormone (FSH). Remarkably, declines in inhibin levels across the menopause transition do not only correlate with an increase in FSH, but also a rapid decrease in bone and muscle mass. Thus, restoration of inhibin function in post-menopausal women may protect from further insult and increase bone health.

Our laboratory is pioneering the development of inhibin mimetics for the treatment of bone disease. Our recently published approach describing the streamlined manufacture of inhibins (Endocrinology, 2016, 157(7), 2799-2809) will enable us to fully explore the contribution of inhibins to reproductive and extra-gonadol functions. This program explores the role of inhibins in reproductive physiology, and the therapeutic potential of inhibins in models of bone disease.

Targeting activin signalling for the treatment of muscle wasting disorders -

Muscle wasting is a fatal consequence of disease progression, and is observed in 80% of patients suffering advanced cancers. Sadly, 25% of all cancer related fatalities are the attributed to tumour-derived wasting effects. Our group has identified a factor, activin, which can promote severe body wasting even in the absence of tumour growth (FASEB J, 2014, 28(4), 1711-1723). Activin is upregulated in many human cancers, and in some instances, is also speculated to contribute to cancer progression. To combat activin-mediated wasting, we have generated a new class of specific antagonists by modification of activins naturally associated propeptide. These propeptides have demonstrated to be both potent and specific antagonists of activin mediated wasting in mice, and have exciting potential in the treatment of cancer-associated wasting in patients suffering cancer cachexia (Molecular Therapy, 2015, 23(3), 434–444). This program explores the tissue and ligand specific targeting of activin-mediated wasting in cancers.