Matrix Microenvironment and Metastasis Laboratory

Our research focus

In collaboration with Australian and international researchers, our research team has developed clinically relevant mouse models of breast cancer metastasis which replicate the entire process of metastasis in patients, from development of a primary tumour in the breast to the spontaneous spread of the disease to bone and brain. Key projects in our laboratory use these models to identify “gene signatures” which can predict patients likely to develop metastases in the brain and other sites, and to test the efficacy of various synthetic inhibitors and natural compounds against bone and brain metastasis.

A particular focus of our laboratory is on investigating whether potent integrin inhibitors found in snake venom can be used to overcome resistance to current therapies or to convert aggressive breast cancers into a milder form of the disease, which is more responsive to drugs already used in the clinic such as anti-oestrogens.

Fast facts

A network of large proteins – called extracellular matrix (ECM) proteins – present in virtually all organs. ECM proteins help maintain the integrity and normal functioning of healthy organs. During cancer development, the expression of these proteins and their receptors on cancer cells (called integrins) is altered to promote survival, growth and homing of cancer cells to distant organs.

Cell surface receptors used by cancer cells to attach to matrix proteins and send signals controlling cancer cell survival, growth and movement.

Our team

Meet our researchers

Metastasis Research Laboratory

Our research focus

We have identified several genes that regulate the metastatic process. By understanding how these genes act to control metastasis, we can develop effective therapies which directly target these genes or other genes controlled by these metastasis regulators. Another important aspect of our research is to examine human breast cancer tissues for evidence that the gene identified in our preclinical models is also relevant in the human disease.

Metastasis Regulating Genes

We have shown that some of the genes we have identified, including caveolin-1, microRNA-200 and BMP4, are able to suppress metastasis. With BMP4, we have found that its metastasis suppressing activity is in part through the inhibition of G-CSF, which controls the mobilisation and differentiation of neutrophils. In the presence of a tumour, the activity of neutrophils can be changed from infection fighting to supporting the spread of cancer cells to other organs, such as the lung. This led to our demonstration in our preclinical models that blocking the mobilisation of neutrophils can reduce metastasis. We are now probing more deeply to understand how neutrophil function is altered by factors released from tumours and the relevance of this to patients with breast cancer.

Much of our research is focused on immune regulation of metastasis by the innate immune system (including macrophages and neutrophils), but some of the other genes we have identified appear to act directly on the tumour cells to prevent their ability to metastasise.

Metastatic Dormancy

Breast cancer is noted for the long latency between diagnosis and therapy for the primary cancer and development of secondary cancers, which can cause ongoing anxiety for patients fearing a recurrence. We are investigating how tumour cells can disseminate from the primary tumour and remain alive but clinically undetectable for many years, and how they start expanding into life-threatening cancers in some patients. We are seeking therapies that prevent the expansion of these dormant cancer cells into new tumours.

Drug Discovery and Delivery

We have collaborated with Dr Ian Street and the Walter and Eliza Hall Institute drug discovery team to identify small molecules that can be developed into drugs to combat metastatic disease. We also work with the ARC Centre of Excellence in Convergent Bio-Nano Science and Technology (Monash University) to improve drug delivery to tumours using nanoparticle technology.

Fast facts

More than 18,000 Australian women and about 150 men were diagnosed with breast cancer in 2019 and more than 3,200 died, largely due to their cancer spreading to other vital organs such as the liver, lung and brain.

The process by which cancer cells spread from one organ to another, forming secondary tumours. Breast cancer commonly spreads to bone, liver, lung and brain.

A common type of white blood cell. They are an important part of the immune system and are found in sites of inflammation. They are the first line of defence against infectious agents but they can also contribute to the growth and spread of tumours.

A nanometre is one billionth of a metre, which means nanoparticles are small enough to move through the bloodstream. Nanotechnology can deliver drugs to specific cells, such as tumour cells, reducing the chances of adverse reactions in the patient.

Recent publications

Cancer Research

Activation of canonical BMP4-Smad7 signaling suppresses breast cancer metastasis.

DOI: 10.1158/0008-5472.CAN-19-0743

View abstract
Nature Reviews Clinical Oncology

A framework for the development of anti-metastatic agents.

DOI: 10.1038/s41571-018-0134-8

View abstract
Cancer Immunology Research

The promotion of breast cancer metastasis caused by inhibition of CSF-1R/CSF-1 signaling is blocked by targeting the G-CSF receptor.

DOI: 10.1158/2326-6066.CIR-13-0190

View abstract

Our team

Meet our researchers

  • Prof Robin Anderson - Head, Translational Breast Cancer Program | Head, Metastasis Research Laboratory Publications
  • Nil Ansari - Postdoctoral Research Fellow
  • Stefan Bader - PhD Student
  • Caroline Bell - Research Assistant
  • Allan Burrows - Postdoctoral Research Fellow Publications
  • Lap Hing (Leo) Chi - PhD Student
  • Bedrich Eckhardt - Postdoctoral Research Fellow Publications

  • Kellie Mouchemore - Postdoctoral Research Fellow Publications Publications
  • Richard Redvers - Postdoctoral Research Fellow Publications
  • Charlotte Roelofs - PhD Student
  • Suraya Roslan - Research Assistant
  • Victoria Simovich - Research Assistant
  • Belinda Yeo - Clinician Scientist Publications

Cell Death and Survival Laboratory

Our research focus


Cellular fate is controlled by multiple molecular pathways. The most studied is apoptosis, a form of programmed cell death used by all multicellular organisms to eliminate cells which are damaged, no longer needed or which might become a threat to the organism. This process is often deregulated in cancer cells allowing them to survive and proliferate when otherwise they should be eliminated.

BH3 mimetics

Dysfunctional apoptosis can cause or accelerate cancer development, but also underlies resistance to common cancer treatment approaches such as chemotherapy. Members of a particular family of proteins (the “BCL-2” proteins) are critical regulators of apoptosis. Recently, a new class of drugs called “BH3 mimetics” have been developed to target some BCL-2 proteins and activate apoptosis, leading to tumour cell death. One of these drugs is now being used in the clinic to treat some blood cancers, and others are under extensive investigation, including by our lab.


Autophagy is predominantly a process that enables cells to survive under stressful conditions such as when nutrients are in short supply. Like apoptosis, it can also become dysfunctional in cancer. Under some circumstance, proteins that regulate autophagy can also interact with those involved in apoptosis. This is a particular interest of our lab as it might have important implications for how cancer cell survive abnormally.

Fast facts

This term encompasses events such as when a cell receives external cues (e.g. from factors like proteins in the blood) and transmits them inside the cell to activate processes such as cell division, movement and death. Cells can also signal to other cells by secreting molecules such as proteins.

Under normal conditions,  apoptosis is essential to remove old, damaged or dangerous cells. In cancer, this process is often switched off allowing abnormal cells to survive and grow when they should otherwise be killed and eliminated.

Primarily, a cell survival process meaning to “self eat”. In times of stress, nutrient deprivation or infection, the cell eats its own components in order to maintain cellular energy levels, or to remove unwanted materials (such as viruses and non-functioning protein aggregates) allowing it to survive.

Recent publications


BCL-XL and MCL-1 Are the Key BCL-2 Family Proteins in Melanoma Cell Survival

DOI: 10.1038/s41419-019-1568-3

View abstract

Structural Insights Into BCL2 Pro-Survival Protein Interactions With the Key Autophagy Regulator BECN1 Following Phosphorylation by STK4/MST1

DOI: 10.1080/15548627.2018.1564557

View abstract
Genes and Development

Physiological Restraint of Bak by Bcl-xL Is Essential for Cell Survival

DOI: 10.1101/gad.279414.116

View abstract

Our team

Meet our researchers

  • A/Prof Doug Fairlie - Head, Cell Death And Survival Laboratory  Publications
  • Erinna Lee - Postdoctoral Research Fellow Publications
  • Tiffany Harris - Research Assistant
  • Nikita Steinohrt - Research Assistant
  • Sharon Tran - PhD Student

Oncogenic Transcription Laboratory

Our research focus

Epigenetic Therapy

We have found that a group of enzymes called histone deacetylases (HDACs) are required for colon cancer cell growth. We have also found that drugs which block these enzymes induce the differentiation and death of colon cancer cells. We are currently working on ways to further improve the anti-tumour activity of these drugs by combining them with existing therapies, in order to develop a new treatment for colon cancer patients.

Differentiation Therapy

Our laboratory also investigates the transcriptional mechanisms by which cellular and tissue differentiation is disturbed during colorectal tumorigenesis. We have identified a number of key transcription factors which are deregulated during this process, and we are using this information to investigate ways differentiation can be reprogrammed in tumour cells.

Discovery of biomarkers to targeted therapies

Through access to clinical trial samples provided by our long-term collaborator A/Prof Niall Tebbutt, our laboratory has a translational research program aimed at discovering the biomarkers predictive response to targeted therapies in gastrointestinal cancers. Agents we are investigating include anti-angiogenic therapeutics (avastin), EGFR inhibitors (cetuximab), BRAF inhibitors and mTOR inhibitors, in the treatment of colorectal cancer, gastric cancer and cholangiocarcinoma.

Fast facts

A small, functional unit of our DNA, containing the information, or “instructions” to produce other functional units, such as proteins.

The process the cell uses to transfer the information contained within the DNA into a format which can be used to inform the production of proteins.

Cancer is a genetic disease. When a gene is mutated, the gene may become unable to provide the right information and instructions to the proteins it informs. The cell is therefore unable to perform its proper job. This can lead to cancer.

Molecules consisting of amino acids, which the cells in the human body need to function properly. Each cell may have thousands of different proteins, each with its own instructions for that cell or those with which it interacts. When the proteins work together they ensure the cell does its job.

Recent publications

Nature Communications

Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity.

DOI: 10.1038/s41467-019-13180-8

View abstract

Genomic Profiling of Biliary Tract Cancer Cell Lines Reveals Molecular Subtypes and Actionable Drug Targets.

DOI: 10.1016/j.isci.2019.10.044

View abstract
Annals of Oncology

The prognostic impact of consensus molecular subtypes (CMS) and its predictive effects for bevacizumab benefit in metastatic colorectal cancer: molecular analysis of the AGITG MAX clinical trial.

DOI: 10.1093/annonc/mdy410

View abstract

Our team

Meet our researchers

  • Prof John Mariadason - Head, Gastrointestinal Cancers Program | Head, Oncogenic Transcription Laboratory Publications
  • Zakia Alam - PhD Student
  • Fiona Chionh - Postdoctoral Research Fellow  Publications
  • George Iatropoulos - PhD Student
  • Laura Jenkins - PhD Student
  • Stan Kacmarczyk - Senior Research Officer

  • Ian Luk - Postdoctoral Research Fellow Publications
  • Irvin Ng - Phd Student
  • Rebecca Nightingale - Research Assistant
  • Kael Schoffer - Research Assistant

Mucosal Immunity and Cancer Laboratory

Our research focus

Function of intestinal immune cells in bowel cancer

Intraepithelial lymphocytes (IELs) are immune cells which continually survey intestinal epithelial cells for infection or damage. Bowel cancer forms when the epithelial cells become damaged and change, growing in an uncontrolled manner. The role of IELs in this process, and whether or not they play a role in tumour cell growth or killing tumour cells, has not been studied in detail. Our laboratory aims to understand these cells, including the molecules that regulate their function in steady state development and in the development of cancer. 

Regulation of cytokines in the gastrointestinal tract

Cytokines, such as IL-17 and IL-22, are secreted by immune cells and are critical in boosting epithelial cell and tumour survival in the intestine. Bowel cancer patients with increased IL-17 and IL-22 levels experience increased tumour growth and have a poorer prognosis. We are dissecting the molecular pathways and cell types involved in regulating IL-17 and IL-22 production to investigate the role these cytokines play in bowel cancer progression. It is crucial that we understand these mechanisms so we can develop new immune cell-mediated therapies to treat gastrointestinal cancers.

Influence of the microbiome on immune health  

Each person’s microbiome is unique and is made up of good bacteria, viruses and fungi which live on the body’s surfaces, such as the skin and intestine. Our understanding of these resident microbes and how they affect the body’s immune response to an infectious organism or disease, such as cancer, is limited. We are working to understand the mechanisms which link the microbiome to overall immune cell health, including the activation of transcription factors that guide immune cell development, as well as the cytokines they secrete in order to communicate with the rest of the body’s cells.

Fast facts

As well as being found in the blood, immune cells are also in the body’s tissues, which they continuously survey for infection and cancer.

Mucus-covered tissues including the lungs and gastrointestinal tract. These sites are home to specialised immune cells, which play a critical role in maintaining mucosal surfaces in order to protect the body from the external environment.

All the bacteria and other microbes that live on the body’s surfaces, such as the skin and intestine. Interaction between these microbes and immune cells is critical in shaping the immune system, and can even influence the body’s response to some cancer treatments.

Recent publications

Trends in Immunology

Control of Lymphocyte Fate, Infection, and Tumor Immunity by TCF-1.
DOI: 10.1016/

View abstract
Journal of Experimental Medicine

TCF-1 limits the formation of Tc17 cells via repression of the MAF-RORγt axis.

DOI: 10.1084/jem.20181778

View abstract
Journal of Experimental Medicine

Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation.

DOI: 10.1084/jem.20121588

View abstract

Our team

Meet our researchers

  • Dr Lisa Mielke - Head, Mucosal Immunology Laboratory Publications
  • Pavitha Parathan - Research Assistant
  • Dinesh Raghu - Postdoctoral Research Fellow Publications
  • Kelly Tran - Research Assistant

Tumour Immunology Laboratory

Our research focus

We constantly use and develop cutting-edge methodologies, including multiplex immuno-fluorescence and RNA-Scope for the characterisation of the tumour microenvironment, protein arrays for the detection of cancer-specific antibodies, and in vitro T cell assays for the detection of novel immunogenic peptides, among others. We are exploring how a successful immune recognition is orchestrated and translated from the early (innate arm) to the late (adaptive) response.

This ‘immunostaging’ of cancers will allow us to understand why and how immunotherapy works for some patients but not for others, and how we can increase the number of patients who benefit from these treatments. The laboratory has extensive experience in clinical trial monitoring and collaborative industry projects, all centred on improving outcomes and quality of life for cancer patients. We collaborate with several leading cancer research laboratories in Australia and internationally.

Fast facts

Tumour cells often look very different to the immune system when compared to healthy cells. To avoid destruction, tumours use a variety of strategies to overcome or to ‘hide’ from an immune response. This interaction of tumour cells with a large variety of immune cells can be more or less pronounced and influence outcome of the disease or response to particular treatments. The quality and quantity of these interactions can be measured on multiple levels, which all together represent the tumour-immune engagement.

Antibodies are proteins produced by a subtype of immune cells which can specifically recognise, bind and often neutralise antigens which the immune system recognises as foreign or a threat (e.g. viruses or bacteria). In cancer, specific antibodies are produced as a response to antigens on cancer cells, which are different than those on normal cells. While their function in the immune recognition of cancer is unclear, their detection in the blood indicates the presence of cancer cells.

Recent publications


Characterising the phenotypic evolution of circulating tumour cells during treatment.
Butyrophilin 2A1 is essential for phosphoantigen reactivity by γδ T cells

DOI: 10.1126/science.aay5516

View abstract
Frontiers in Immunology

Autoantibodies May Predict Immune-Related Toxicity: Results from a Phase I Study of Intralesional Bacillus Calmette-Guérin followed by Ipilimumab in Patients with Advanced Metastatic Melanoma.

DOI: 10.3389/fimmu.2018.00411

View abstract
Nature Communication

Characterising the phenotypic evolution of circulating tumour cells during treatment.

DOI: 10.1038/s41467-018-03725-8

View abstract

Our team

Meet our researchers

Cancer Therapeutics Development Group

Our research focus

Our main research areas are metastatic gastrointestinal and breast cancers.  We focus on how inflammation drives the progression to advanced disease and how new treatments could be designed to block its harmful effects.

Understanding how pro-inflammatory pathways drive tumour progression

Inflammatory cytokines make cancer cells more prone to growth and spreading to other parts of the body. By understanding how pro-inflammatory cytokines cause these cellular effects, we have been able to identify molecular targets, for which we are now developing targeted treatments.

Cancer drug discovery

Our research has led to the identification of particular inflammatory pathways, which we now aim to target so we can develop specific treatments which will block cancer growth in the gastrointestinal tract. Working with structural biologists and chemists, we have identified new compounds which we are testing for their ability to block tumour cell survival and spread to other sites in the body. These can then be used in clinical research to provide new treatment options for patients.

Repurposing of commonly used drugs as new cancer treatments

New drug development is a lengthy and resource-intensive process. It makes sense to reassess existing drugs for additional uses at the same time as researching new drug development. We are investigating the therapeutic value of a drug, already clinically approved to treat osteoporosis, as a novel treatment in gastric and colon cancers.

Interaction between the intestinal barrier and the microbiome

We are studying the effects of inflammatory disruption on the intestinal barrier in host-microbiome interaction and how this may contribute to the development of colon cancer. Our team is also exploring the mechanisms of the gut microbiota so that its metabolites may be reinstated following chemotherapy and immunotherapy treatment in cancer patients.

Fast facts

When newly-developed novel compounds are first tested for anti-cancer capabilities using a range of biochemical and cell-based assays.

The body’s natural response to tissue damage, infection and disease.

Different cell types of the body produce pro-inflammatory cytokines as a way of causing inflammation to repair tissue and fight infection.

All the trillions of microorganisms and their genetic material present in the intestinal tract. Mainly comprising bacteria, they play a key role in functions critical to our health.

Recent publications

EMBO Molecular Medicine

Repurposing the selective estrogen receptor modulator bazedoxifene to suppress gastrointestinal cancer growth.

DOI: 10.15252/emmm.201809539

View abstract
Seminars in Cancer Biology

Repurposing of drugs as STAT3 inhibitors for cancer therapy.

DOI: 10.1016/j.semcancer.2019.09.022

View abstract
Pharmacology & Therapeutics

Evaluating the benefits of renin-angiotensin system inhibitors as cancer treatments.

DOI: 10.1016/j.pharmthera.2020.107527

View abstract

Our team

Meet our researchers

Tumour Microenvironment and Cancer Signaling Group

Our research focus


DCLK1 is a microtubule-associated protein which catalyses the polymerisation of tubulin dimers. This process is critical in the formation of microtubules, a major component of the cellular cytoskeleton, and also important in many cellular functions such as cell division and migration. DCLK1 expression is excessively upregulated in various types of cancer and, pertinently, high DCLK1 expression is significantly correlated with poorly differentiated cancers, lymph node metastasis, advanced clinical stage, and poorer overall patient survival, suggesting that the overexpression of DCLK1 may accelerate cancer development.

Tuft cells

A structurally unique cell type, best characterised by striking microvilli which form an apical tuft. These cells represent approximately 0.5% of tissue epithelial cells depending on location. Tuft cells act as luminal sensors, linking the luminal microbiome to the host immune system, which may make them a potent clinical target for modulating host response to a variety of acute or chronic immune-driven conditions.

Our lab is using powerful single-cell sequencing approaches and has developed experimentally tractable tools in order to interrogate this rare cell population, with the aim of unravelling its physiological importance in inflammation-driven gastrointestinal diseases, such as colon and gastric cancers.

Innate lymphoid cells

These cells are a newly discovered type of innate immune cell which resemble lymphocytes but lack a T cell receptor. They are predominantly found in mucosal surfaces associated with epithelial tissues, such as the gut, lung and skin, and have important roles in immunity, infection and homeostasis. Our lab is investigating the interplay between Tuft cells and ILC2 cells during gastric homeostasis and cancer.

Fast facts

The cellular environment within which the tumour exists. This includes the surrounding blood vessels, immune cells, fibroblasts, bone marrow-derived inflammatory cells, lymphocytes, signalling molecules and the extracellular matrix (ECM).

Rare chemosensory cells scattered throughout the epithelium tissue of the digestive tract. Their biological functions include tissue repair and regeneration, as well as modulation of immune responses during parasite infections. Tuft cell numbers increase during the early stages of tumour development. The importance of this increase is not yet well understood.

They play a crucial role of secreting type 2 cytokines in response to certain parasitic infections. They have also been implicated in the development of allergic lung inflammation. They express characteristic surface markers and receptors for chemokines, which are involved in distributing lymphoid cells to specific organ sites. ILC2s are critical in primary responses to local Th2 antigens, such as helminths and viruses, and is why they are abundant in tissues of the skin, lungs, liver and gut. Their role in cancer development is not yet well understood.

The epithelial–mesenchymal transition (EMT) is a process through which epithelial cells lose their cell polarity and intercellular adhesion, instead gaining migratory and invasive properties to become mesenchymal stem cells, which are multipotent stromal cells that can differentiate into a variety of different cell types.

Our team

Meet our researchers

Cancer and Inflammation Laboratory

Our research focus

We focus our research on three approaches to interfere with the communication between cancer and normal cells within a tumour.

Stat3 and tumourigenesis

Pronounced epithelial Stat3 activity is not only observed during wound-healing, but also in a majority of cancers including those in the colon, stomach, breast and lung. Our lab recently established a novel link, showing that the cytokine interleukin (IL)-11 – through its shared gp130 receptor, the associated Jak kinases and Stat3 signaling – promotes tumourigenesis. Surprisingly, this signaling cascade also becomes rate limiting for the growth of colon and gastric tumours that are driven by mutations in well recognised cancer pathways.

Neoplastic cells

We are therapeutically exploiting that neoplastic cells have often developed a higher dependency on a particular signal than their normal counterparts. For instance, oncogenic activation of the WNT/beta-catenin signaling cascade is the most common tumour-initiating event that occurs in epithelial stem cells and results in the development of sporadic colorectal cancer. Because interference with the gp130/Stat3 signaling cascades limits the expansion of such intestinal (cancer) stem cells, the addiction of colon cancer cells to gp130/Stat3 signaling can be therapeutically exploited in these tumours where targeting of the mutated WNT/beta-catenin signaling cascade is not feasible.

Hck activation

The cellular composition of the tumour microenvironment affects how well a tumour can grow and respond to targeted and immune-modulatory therapy. Although these processes are affected by many different cell types within the tumour stroma, macrophages and other myeloid-derived cells are among the most important players. We have found that the myeloid cell kinase Hck is highly abundant in the tumour microenvironment and aberrant Hck activation suppresses an effective anti-tumour immune response. We are therefore identifying ways by which we can most effectively target Hck to restore and augment anti-tumour immune responses to more effectively kill the cancer cells.

Fast facts

Cancer cells have hijacked for their own benefit the inflammatory processes that help support wound-healing of normal tissues.

Within the tumour there are a number of cell types, both cancer cells and non-cancer cell types. This collective of different cell types is characterised by many molecular interactions that collectively determine how well a tumour responds to treatment.

A gene or protein which is identified to cause, or play a major role, in the disease.

A drug which attacks a specific protein of the cancer. Such drugs therefore only work on cancer where such a protein confers a specific benefit for a particular cancer to grow and spread.

Recent publications

Cancer Cell

Inhibition of Hematopoietic Cell Kinase Activity Suppresses Myeloid Cells-Mediated Colon Cancer Progression.

DOI: 10.1016/j.ccell.2017.03.006

View abstract
Nature Communications

IL33-mediated mast cell activation promotes gastric cancer through macrophage mobilization.

DOI: 10.1038/s41467-019-10676-1 (2019)

View abstract
Nature Reviews Cancer

Therapeutically exploiting STAT3 activity in cancer – using tissue repair as a road map.

DOI: 10.1038/s41568-018-0090-8 (2019)

View abstract

Our team

Meet our researchers

  • Prof Matthias Ernst - Director, ONJCRI | Head, Cancer And Inflammation Program |
    Head, Cancer And Inflammation Laboratory | Head, School Of Cancer Medicine, La Trobe University Publications
  • Shoukat Afshar-Sterle - Research Assistant Publications
  • Amr Allam - Postdoctoral Research Fellow Publications
  • Mariah Alorro - PhD Student
  • David Baloyan - Flow Cytometry Operator Publications
  • Christine Dijkstra - Research Assistant
  • Belinda Duscio - Research Assistant
  • Moritz Eissmann - Postdoctoral Research Fellow Publications
  • Gangadhara Gangadhara - Postdoctoral Research Fellow Publications

  • Anne Huber - PhD Student
  • Jennifer Huynh - Postdoctoral Research Fellow Publications
  • Saumya Jacob (Parambate) - Research Assistant
  • Riley Morrow - PhD Student
  • Megan O'Brien - Research Assistant
  • Lokmand Pang - PhD Student
  • Ashleigh Poh - Postdoctoral Research Fellow Publications
  • Angela Sanchez Hormigo – Scientist Publications

Our Research

Our research programs focus on developing treatments for a range of cancers including breast, bowel and gastrointestinal tract, liver, lung, skin and brain cancer.


Program Head: Prof Matthias Ernst

Understanding how normal cells in the body can become corrupted by tumour cells is critical in order to stop the growth and spreading of cancers.

Many of the molecular processes that cancer cells use to communicate with normal cells also play important roles during wound-healing.

Therefore, cancer cells often hijack some of these mechanisms in order to survive, grow, obtain a steady stream of nutrients and develop resistance to treatment.

Our Cancer and Inflammation Program aims to better understand how cancer cells and normal cells communicate with each other within the tumour environment.

If we can disrupt these lines of communication, cancer cells will be more vulnerable as they become less supported by the normal cells in their vicinity.

Importantly, this strategy may also help make tumour cells more visible to immune cells and therefore more vulnerable to treatment with contemporary immune-based therapies.

While the activities of our Program focus primarily on cancers of the bowel, stomach and breast, many of these molecular communication mechanisms are also found in other solid tumours.

Therefore, the insights gained from our research could ultimately be translated to many different solid malignancies.

Find out more about the Laboratory and Groups within the Cancer and Inflammation Program:

Cancer and Inflammation Laboratory
Prof Matthias Ernst
Tumour Microenvironment and Cancer Signaling Group
Dr Michael Buchert
Cancer Therapeutics Development Group
Dr Ashwini Chand


Program Head: Prof Jonathan Cebon

Research from the Cancer Immunobiology Program is producing life-saving results by better understanding the role of the immune system in cancer treatment.

Our researchers are harnessing the power of the body’s immune system to treat cancer by performing clinical trials with drugs which stimulate immune responses.

We are also developing diagnostic tests to better select patients for immunotherapy, and predict and manage auto-immune side effects.

Both cancer and the immune system change with time – indeed they can shape each other. As immunity attacks, the cancer can adapt and escape immune recognition.

The cancer can also interfere with immune system cells in a variety of ways.

We are particularly interested in understanding the targets which the immune system recognises, and how both cancer and immunity co-evolve, to allow us to discover new therapeutic targets.

Find out more about the laboratories  within the Cancer Immunobiology Program:

Tumour Immunology Laboratory
Dr Andreas Behren
Mucosal Immunity and Cancer Laboratory
Dr Lisa Mielke


Program Head: Prof John Mariadason

Our Gastrointestinal Cancer Program team investigates the biological causes of cancers of the colon (bowel), biliary tract and stomach, to develop new treatments for patients affected by these diseases. We are particularly focused on identifying and targeting major proteins that enable tumour cells to survive in the body, and are testing whether drugs which work in other cancers can be re-purposed for treatment of gastrointestinal cancers.

Within this program we are investigating the molecular mechanisms which disturb cellular differentiation, proliferation and survival, and cause or perpetuate cancer. Our research focuses on transcriptional and epigenetic mechanisms, and also aims to discover biomarkers to better tailor therapies to cancer patients.

We want to understand the biological causes of cancers of the colon (bowel), biliary tract and stomach so that new treatments can be developed. We also aim to identify and target the major “pro-survival” proteins in these tumours and are testing if drugs that target the “epigenome” can prevent the growth and spread of these cancers.

Find out more about the laboratories within the Gastrointestinal Cancer Program:

Oncogenic Transcription Laboratory
Prof John Mariadason
Cell Death and Survival Laboratory
A/Prof Doug Fairlie


Program Head: Prof Robin Anderson

The Translational Breast Cancer Program focuses on reducing breast cancer deaths that are caused mainly by the spread of the disease to other organs – a process called metastasis.

We are seeking a mechanistic understanding of how cells leave the primary breast tumour and travel to tissues such as the lung or bone and establish as secondary tumours. We track cancer cells as they move through the bloodstream, identifying the cancer cells with the greatest ability to form a secondary tumour. We investigate how they adapt to growth in their new environments, such as bone or lung or brain, relying on support from normal cells in their new home.  The genes that we have identified as controlling these events are now targets for therapies that we are developing to inhibit the growth of secondary breast cancer.


Program Head: Prof Andrew Scott AM

The Tumour Targeting Program focuses on the targeting, molecular imaging and treatment of tumours, as well as defining receptor-based signaling pathways responsible for cancer cell growth, and to uncover mechanisms that result in resistance to targeted therapies.

Our program also aims to identify novel targets for cancer drug development which are suited for antibody-based therapy and visualisation of cancer cells. Through sophisticated protein engineering and molecular imaging techniques, novel diagnostic and therapeutic approaches to a range of cancers are being developed, and extended into clinical studies in cancer patients.

Find out more about the laboratories and groups within the Tumour Targeting Program:

Tumour Targeting Laboratory
Prof Andrew Scott AM
Receptor Biology Laboratory
A/Prof Peter Janes


The Centre for Research Excellence (CRE) in Brain Cancer was established through $2 Million funding from the Victorian Cancer Agency. Led by Professors Andrew Scott AM and Hui Gan, the CRE is aimed to develop innovative approaches for diagnosing and treating brain cancers, and to take new discoveries into clinical trials in brain cancer patients.

The principal research themes of the CRE in Brain Cancer are:

  1. Developing novel imaging probes: to assist with improved diagnosis and prognostication, better treatment selection and more accurate assessment of
  2. Developing new molecular assays: for better characterisation of brain cancers, leading to improved decision making and selecting the most appropriate treatment for patients.
  3. Developing new drugs and approaches to treatment, which will result in improved responses and survival in brain cancer patients.

This research utilised our access within the ONJCRI, and through collaborations in Australia and internationally, to cutting edge research platforms in genomics, immunology, brain cancer model systems, molecular imaging, and therapeutics development. Our collaborators include the Victorian Comprehensive Cancer Centre (VCCC) brain tumour group, the Cooperative Trials Group For Neuro-Oncology (COGNO), the Australasian Radiopharmaceutical Clinical Trials Network (ARTnet), and the Glioma Longitudinal Analysis (GLASS) Consortium.

In addition to the scientific and clinical aims of the CRE in Brain Cancer, education and training are key components of the overall program.

The Centre is co-led by Prof Andrew Scott AM and Prof Hui Gan


The Bioinformatics and Cancer Genomics (BCG) Laboratory was recently established to support the bioinformatics needs at the Olivia Newton-John Cancer Research Institute. The BCG Laboratory is internationally recognised as a leading group in developing state-of-the-art bioinformatics tools for analysing genomics data including next-generation and third-generation sequencing data.

Our Laboratory’s research themes include:

  1. Map and quantify expression data generated from single-cell and bulk RNA sequencing
  2. Discover genomic mutations including structural variants in cancer genomes
  3. Use genomics data to understand the molecular mechanisms underlying development of cancer and immune diseases
  4. Use machine learning algorithm to predict the prognosis and drug response of various types of cancer

Our team collaborates with many laboratories and groups at ONJCRI. We also collaborate with laboratories from other institutes including Doherty Institute, Walter and Eliza Hall Institute, Diamantina Institute and Peter MacCallum Cancer Centre. We also collaborates with clinicians from various hospitals.

Our team also provides bioinformatics consultations and workshop training to students and staff at the ONJCRI.

The BCG Laboratory is led by Prof Wei Shi