Associate Professor Nicholas Andrew Saunders

Dr of Philosophy, Bachelor of Science (Honours)

Principal Research Fellow


Understanding the molecular basis for the control of squamous differentiation

Understanding how these processes are dysregulated during the development of oral and skin cancers

Exploiting this knowledge in the development of novel treatments for skin cancers and oral cancer

Interrogating chemotherapeutic sensitivity

Identifying novel strategies to treat metastatic osteosarcoma

About me

"Wonderment in nature."That's how Associate Professor Nick Saunders describes what has driven his interest in science ever since a young age. This sense of wonder at the inner-workings of nature led him to the University of Western Australia (UWA) where he first studied anatomy and human biology, and then trained as a pharmacologist.

His PhD studies in pharmacology engendered a profound interest in the molecular sciences. Saunders wanted to learn more. He soon found an opportunity to do so when he was awarded a Fogarty Visiting Fellowship at the National Institute of Environmental Health Sciences (NIEHS) in the US.It was there, in the laboratory of Professor Anton Jetten, that Saunders first began working on squamous epithelial cells. These cells are found on the outer layer of the skin and upper aerodigestive tract.  Saunders and Jetten were particularly interested in cell ‘differentiation’, which is the normal process by which cells mature and become specialised. By studying squamous cell differentiation in both normal and cancerous conditions, they wanted to identify the early triggers that cause things to go awry in Squamous Cell Carcinoma (SCC).  SCC is a common form of skin cancer and accounts for approximately 90% of head and neck cancers. Saunders recognised that understanding differentiation in SCC is not only crucial to the development of new SCC therapeutics, it has even broader implications.  “SCC has interesting biology," he explains. "It provides an opportunity to study the cancer process.”Saunders and his NIEHS colleagues were able to begin painting a picture of the molecular players in SCC development and he quickly became an expert on keratinocytes, the epithelial cell type that comprises stratified squamous epithelia. This drew the interest Professor Ian Frazer at the University of Queensland’s Centre for Immunology and Cancer Research (CICR) and Saunders was offered the opportunity to establish an Epithelial Pathobiology Group at the CICR.  Saunders is now an Associate Professor and Head of the Epithelial Cancer Division at the University of Queensland's Diamantina Institute (UQDI), and believes the unique relationship between UQDI and the Princess Alexandra Hospital is essential to the success of his research programs.  "We try to engage in aspects of cancers that represent the biggest clinical challenge," he says. "We are entirely dependent on clinical collaborations. I couldn't do this work elsewhere."  Specifically, Saunders wants to exploit defects in cell development in order to develop new diagnostics and therapeutics for SCC. A major step toward this goal relates to a protein called E2F, which is an essential component of normal cell development and growth.  Saunders and his colleagues found that E2F is produced at higher than normal levels in SCC, and when that happens, the cells lose the ability to regulate growth and proliferation. Saunders is investigating new anti-cancer strategies for SCC based on this discovery.   He is also particularly interested in another form of cancer called osteosarcoma, the most common form of paediatric bone cancer. He and colleague, Dr Endo-Munoz,  have discovered that the loss of bone cells called osteoclasts is what allows an osteosarcoma to metastasise to other organs such as the lungs. This is a crucial finding, because it is metastasis that allows osteosarcoma to become life threatening.  His goal now is to find the precise molecular trigger that causes this loss of osteoclasts, then find a way to block it. The outcomes of this work could lead to applications in other forms of metastatic cancer.  When asked what it would mean if metastasis could be targeted therapeutically, Saunders replies, "It will mean finding cures for what are considered incurable diseases."


Recent Publications1. Walshe J, Serewko-Auret MM, Teakle N, Cameron S, Minto K, Smith L, Burcham PC, Russell CT, Strutton G, Griffin A, Chu FF, Esworthy S, Reeve VE, Saunders NA. Inactivation of glutathione peroxidise activity contributes to UV-induced squamous cell carcinoma formation. Cancer Res. 67:4751-4758, 2007, IF = 8.62. Dahler AL, Rickwood D, Guminski A, Teakle N, Saunders NA. Indole-3-carbinol – induced growth inhibition can be converted to a cytotoxic response in the presence of TPA + Ca2+ in squamous cell carcinoma cell lines. FEBS Letters, 581(20):3839-3847, 2007. IF = 3.43. Wang XQ, Hayes MT, Kempf M, Fraser JF, Liu A, Cuttle L, Friend L, Rothnagel JA, Saunders NA, Kimble RM. Fetuin A: A major fetal serum protein that promotes “wound closure” and scarless healing. J. Invest. Dermatol., 128(3):753-7, 2008. IF = 4.94. Erlich RB, Rickwood D, Coman W, Saunders NA, Guminski A. Valproic acid as a therapeutic agent for head and neck squamous. Cancer Chemotherapy and Pharmacology. 63(3):381-389, 2008. IF = 2.65. Endo-Munoz L, Dahler A, Teakle N, Rickwood D, Hazar-Rethinam M, Abdul-Jabbar I, Sommerville S, Dickinson I, Kaur P, Paquet-Fifield S, Saunders NA. E2F7 can regulate proliferation, differentiation and apoptosis in human keratinocytes: implications for cutaneous squamous cell carcinoma formation. Cancer Res.,69(5):1800-1808, 2009 IF = 7.76. Paquet-Fifield S, Schlueter H, Li A, Aitken T, , Gangatirkar P, Blashki D, Koelmeyer R, Pouliot N, Patsides M, Ellis S, Brouard N, Zannettino A, Saunders N, Thompson N, Li J, Kaur P. A role for pericytes as microenvironmental regulators of epithelial tissue regeneration in human skin. J. Clin. Invest., 119(9):2795-2806, 2009. IF= 16.97. Endo-Munoz L, Cumming A, Sommerville S, Dickinson I, Saunders NA. Osteosarcoma is characterised by reduced expression of markers of osteoclastogenesis and impaired antigen presentation compared to normal bone. Br. J. Cancer, 103(1):73-81, 2010. IF = 4.88. Cameron S, Dahler A, Jabbar I, Endo-Munoz L,Thomas G, Poth K, Rickwood D, Guminski A, Saunders N. Tumour initiating activity and tumour morphology of HNSCC is modulated by interactions between clonal variants within the tumour. Lab Invest. In Press. IF = 4.6 (This manuscript was the topic of the editorial commentary in the same edition of the journal)9. Poth K, Guminski A, Thomas G, Jabbar I, Saunders NA. Treatment with cisplatin induces a transient increase in tumourigenic potential in resistant HNSCC cells. Mol. Cancer Ther. 9(8):2430-2439, 2010. IF = 5.410. Endo-Munoz L, Cumming A, Rickwood D, Wilson D, Cueva C, Ng C, Strutton G, Cassady I, Evdokiou A, Sommerville S, Dickinson I, Guminski A, Saunders NA. ACP5/TRAP downregulation and the absence of osteoclasts is a feature of osteosarcoma and predicts progression to metastasis. Cancer Research. 70(18):7063-7072, 2010. IF = 8.2