Dr Lucy Barrett1,2, Dr Jason Waithman1, Dr Vanessa Fear1, Professor Fiona M Wood3,4,5, Dr Mark Fear3,4

1Telethon Kids Institute, Perth, Australia, 2Institute for Respiratory Health, Perth, Australia, 3Burn injury research unit, School of Biomedical Sciences, University of Western Australia, Perth, Australia, 4Fiona Wood Foundation, Perth, Australia, 5Burns Service of Western Australia, WA Department of Health, Perth, Australia

Abstract:

Burn injury is a major public health issue, and while advances in acute care have significantly improved survival and patient outcomes, recent studies using long-term hospital data from burn patients in Western Australia and Scotland with over 30 years follow-up have shown that burns are associated with an increase in rates of cancer. Evidence from our research strongly suggests that immune dysfunction induced by burn injury persists long-term, leading to a chronic suppression of the immune system. The immune system is known to play an important role in cancer control and prevention, and we hypothesise that this sustained immune dysfunction leads to the observed increase in cancer incidence in burn patients.

In order to investigate this link, we tested three different models of tumour development in combination with our established murine model of non-severe burn injury. Whilst no significant difference in primary tumour growth was observed using a B16 melanoma model, an epicutaneous model of tumour growth with limited penetrance demonstrated a significant increase in tumour development in comparison to sham injured control mice. Our results support the population studies suggesting burn injury leads to increased susceptibility to cancer. This model will now be used for future mechanistic studies, in which we aim to gain a better understanding of the mechanisms underlying increased susceptibility to cancer after burn injury.


Biography:

Dr Barrett is an early-career researcher with a particular interest in understanding how burn injury can have long-term impacts on patient health through disruption of cellular and molecular functions.