Professor Leonie Quinn

1999 PhD, School of Medicine, Flinders University of South Australia.
ANU College of Health and Medicine

Areas of expertise

  • Cell And Nuclear Division 060402
  • Gene Expression (Incl. Microarray And Other Genome Wide Approaches) 060405
  • Genetics 0604
  • Cancer Cell Biology 111201
  • Cell Development, Proliferation And Death 060103
  • Developmental Genetics (Incl. Sex Determination) 060403

Research interests

Dr Quinn’s research uses Drosophila molecular genetic approaches to determine how transcriptional networks integrate extra- and intracellular signalling inputs to drive tissue growth. Deciphering pathways controlling growth during normal development provides an avenue to understanding dysregulation of these networks in cancer. 


After completing her PhD studies in Adelaide (1999) and conducting postdoctoral research at the Peter MacCallum Cancer Centre in (2000-2007), Dr Quinn established her laboratory at the University of Melbourne in 2007. In 2016 Dr Quinn relocated to the John Curtin School of Medical Research (ANU, Canberra) to establish the Drosophila Cancer Models Group in the Department of Cancer Biology and Therapeutics.


Researcher's projects

Developmental Cancer Models Projects

Dr Quinn’s current research involves generating genetic models using the vinegar fly (Drosophila Melanogaster) to understand the initiation and progression of human cancer. Her core research uses in vivo cancer models to determine how complex developmental signalling pathways are integrated into transcriptional networks. In particular we aim to understand how these networks coordinate cell growth and division to establish the body plan during development, and also maintain tissue homeostasis in adult animals; as cell growth and proliferation are invariably dysregulated in human cancer. Her group also has a strong interest in using in vivo stem cell models to determine the mechanism(s) by which the stem cell microenvironment or “niche” regulates stem and progenitor cell growth, division and differentiation. 


Available student projects

Project 1 - Transcriptional control of the MYC oncogene

One core regulator of growth and division of great interest to our research is the MYC oncogene, which is a potent activator of cell growth networks and upregulated in most human cancers. As therapeutically targeting MYC itself has proved unfeasible, we need to find new ways to indirectly target MYC in cancer. Most MYC-driven cancer is due to upregulation of expression, but the networks controlling MYC transcription in malignancy are largely unknown. The single stranded DNA binding proteins FBP and FIR are essential for transcriptional control of the MYC oncogene, and dysregulation of this network is linked with a wide variety of cancers, eg. kidney, breast, liver, lung, bladder, prostate, gastrointestinal and brain. This research aims to use a combination of in vivo genetic models (Drosophila and mouse) and human cancer models to unravel the mechanisms for regulation of MYC expression by FBP/FIR.


Project 2 – Brain tumour models

With no effective drug treatments for malignant glioma these tumours are invariably lethal. One key discovery in glioma biology is that the EGFR/RAS/PI3K axis is activated in most gliomas. Indeed, preclinical trials are underway for therapeutics targeting PI3K/AKT and RAS/RAF in malignant glioma. Unfortunately, these studies have already revealed rapid acquisition of tumour resistance, which highlights the importance of understanding the activity of downstream targets. Elevated FBP and MYC correlate with poor patient survival, which suggests FBP and MYC abundance/activity might also be drivers of glioma malignancy. This project builds on our exciting observation that FBP is a critical downstream target of EGFR/RAS/PI3K. We aim to use Drosophila, mouse and human glioma models to determine how the FBP-MYC axis drives MYC expression and brain tumour growth. Given the capacity of FBP knockdown to extinguish RAS-activated MYC expression, we propose that FBP is an attractive future target for developing novel cancer therapies. 

Project 3 – Leukemia Models

Ribosomal proteins (Rps) are essential for functional ribosomes, protein synthesis, and proliferative cell growth. Paradoxically, mutation of Rps can actually promote growth and proliferation and, in some cases, bestow predisposition to cancer. Our work provided the first rationale to explain the counter-intuitive organ overgrowth phenotypes observed for Drosophila Rp mutants by revealing that Rp mutants can drive tissue overgrowth cell extrinsically, whereby reduced Rps in the hormone-secreting gland of the larvae decreases activity of the steroid hormone ecdysone, extending the growth phase of development and causing tissue overgrowth. This project aims to extend these studies to better understand how Rp mutations cause the hypoplastic anemia associated with the human leukemia. Thus we have developed Drosophila models to specifically reduce Rps in the hematopoietic system to gain novel insights into how Rp mutations can promote leukemia in humans. This project will provide much needed insight into the processes linking reduced levels of Rps to cancer predisposition.


Project 4 - Cancer stem cell models

The discovery of cancer stem cells emphasized the importance of interactions between stem cells and their microenvironment. More than 2 decades of research in Drosophila have documented the capacity of the supporting cellular microenvironment or “niche” in orchestrating renewal and differentiation of stem cell populations. In the context of cancer, we expect proper organisation of the cellular microenvironment will also be essential for preventing tumour formation. However, this area of cancer biology has remained enigmatic due to the difficulty in tracing interactions between human tumours and their niche in mammals. This project will extend on our exciting observations that loss of the MYC repressor Hfp/FIR from the Drosophila ovarian stem cell niche generates germline tumours far from the local niche. We aim to extend these observations to human and mouse models to begin dissecting contributions of the tumour microenvironment to initiation and progression of ovarian cancer. 



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Updated:  21 June 2024 / Responsible Officer:  Director (Research Services Division) / Page Contact:  Researchers