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- A complete cure for HBV
- A stable efficacious Toxoplasma vaccine
- Activating SMCHD1 to treat FSHD
- Improving vision outcomes in retinal detachment
- Intercepting inflammation with RIPK2 inhibitors
- Novel inhibitors for the treatment of lupus
- Novel malaria vaccine
- Precision epigenetics silencing SMCHD1 to treat Prader Willi Syndrome
- Rethinking CD52 a therapy for autoimmune disease
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- Anne-Laure Puaux
- Associate Profesor Ian Majewski
- Associate Professor Aaron Jex
- Associate Professor Alyssa Barry
- Associate Professor Andrew Webb
- Associate Professor Chris Tonkin
- Associate Professor Daniel Gray
- Associate Professor Diana Hansen
- Associate Professor Edwin Hawkins
- Associate Professor Emma Josefsson
- Associate Professor Ethan Goddard-Borger
- Associate Professor Grant Dewson
- Associate Professor Isabelle Lucet
- Associate Professor James Murphy
- Associate Professor James Vince
- Associate Professor Jason Tye-Din
- Associate Professor Jeanne Tie
- Associate Professor Jeff Babon
- Associate Professor Joan Heath
- Associate Professor Justin Boddey
- Associate Professor Kate Sutherland
- Associate Professor Leanne Robinson
- Associate Professor Marco Herold Marco Herold
- Associate Professor Marie-Liesse Asselin-Labat
- Associate Professor Matthew Ritchie
- Associate Professor Melissa Davis
- Associate Professor Misty Jenkins
- Associate Professor Nawaf Yassi
- Associate Professor Oliver Sieber
- Associate Professor Peter Czabotar
- Associate Professor Rachel Wong
- Associate Professor Rhys Allan
- Associate Professor Rosie Watson
- Associate Professor Ruth Kluck
- Associate Professor Sandra Nicholson
- Associate Professor Sant-Rayn Pasricha
- Associate Professor Seth Masters
- Associate Professor Sumitra Ananda
- Associate Professor Tim Thomas
- Associate Professor Wai-Hong Tham
- Associate Professor Wei Shi
- Catherine Parker
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- Dr Alisa Glukhova
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- Professor Leonard C Harrison
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- Professor Terry Speed
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- Professor Warren Alexander
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- A new regulator of stemness to create dendritic cell factories for immunotherapy
- Advanced methods for genomic rearrangement detection
- Control of cytokine signaling by SOCS1
- Defining the protein modifications associated with respiratory disease
- Delineating the pathways driving cancer development and therapy resistance
- Developing a new drug that targets plasmacytoid dendritic cells for the treatment of lupus
- Development and mechanism of action of novel antimalarials
- Development of a novel particle-based malaria vaccine
- Development of tau-specific therapeutic and diagnostic antibodies
- Discovering novel therapies for major human pathogens
- Dissecting host cell invasion by the diarrhoeal pathogen Cryptosporidium
- Epigenetic biomarkers of tuberculosis infection
- Essential role of glycobiology in malaria parasites
- Evolution of haematopoiesis in vertebrates
- Human lung protective immunity to tuberculosis
- Identifying novel treatment options for ovarian carcinosarcoma
- Interaction with Toxoplasma parasites and the brain
- Interactions between tumour cells and their microenvironment in non-small cell lung cancer
- Investigating the role of mutant p53 in cancer
- Microbiome strain-level analysis using long read sequencing
- Minimising rheumatic adverse events of checkpoint inhibitor cancer therapy
- Modelling spatial and demographic heterogeneity of malaria transmission risk
- Naturally acquired immune response to malaria parasites
- Predicting the effect of non-coding structural variants in cancer
- Structural basis of catenin-independent Wnt signalling
- Structure and biology of proteins essential for Toxoplasma parasite invasion
- T lymphocytes: how memories are made
- TICKER: A cell history recorder for longitudinal patient monitoring
- Targeting host pathways to develop new broad-spectrum antiviral drugs
- Targeting post-translational modifications to disrupting the function of secreted proteins
- Targeting the epigenome to rewire pro-allergic T cells
- Targeting the immune microenvironment to treat KRAS-mutant adenocarcinoma
- The E3 ubiquitin ligase Parkin and mitophagy in Parkinson’s disease
- The molecular controls on dendritic cell development
- Understanding malaria infection dynamics
- Understanding the genetics of neutrophil maturation
- Understanding the neuroimmune regulation of innate immunity
- Understanding the proteins that regulate programmed cell death at the molecular level
- Using cutting-edge single cell tools to understand the origins of cancer
- When healthy cells turn bad: how immune responses can transition to lymphoma
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About cancer

Cancer is a disease caused by uncontrollably growing cells. Cancer will affect 1 in 3 Australians during their lifetime. Although some types of cancer can be cured, for others there are few effective treatments.
More than 400 of our researchers are working to improve the health of people with cancer.
Our cancer research
Our scientists are working on many aspects of cancer research including:
- Understanding the process through which cells become cancerous.
- Revealing the molecules that underlie the growth, longevity and progression of cancers.
- Designing potential new treatments for cancer or methods of cancer prevention.
- Developing new ways to detect and diagnose cancer.
- Testing the effectiveness of new treatment and detection strategies for cancer, including through clinical trials.
Our researchers focus on many of the most significant cancers in Australia and globally, including
- Leukemia and lymphoma (cancers of blood cells)
- Brain cancer
- Breast cancer
- Bowel cancer
- Lung cancer
- Ovarian cancer
- Stomach cancer
- Pancreatic cancer
What is cancer?
Cancer occurs when a cell develops changes that allow it to grow abnormally. This causes illness when cancer cells prevent the normal, essential functioning of the body’s organs, such as:
- Taking up space that was occupied by normal cells, preventing the function of body organs.
- Diverting blood, nutrients and other resources to the cancer cell, starving the normal cells.
- Secreting substances that change the behaviour of normal cells in the body.
Cancers are often named to reflect the body organ from which they develop. Some cancers are named for the cell type from which they come, for example, leukaemia is a cancer of leukocytes (also known as white blood cells).
Many cancers start growing as a lump, called a tumour, in one part of the body. Cancers of blood cells (leukaemia) often do not form a tumour.
Some cancer cells may develop the ability to spread (metastasise) to other parts of the body.
Cancer Australia has detailed information on how cancers are named.
What causes cancer?
Cancer occurs when a normal cell accumulates changes to its genetic material (DNA) that make the cell divide uncontrollably. The cell fails to respond to the normal safeguards that restrict normal cell growth.
Our cancer biology page provides more information about how cancer develops.
Many cancer-associated changes to genes have been identified. Broadly, genes that may be changed in cancer cells can be considered either:
- Cancer promoting: ‘oncogenes’, over-active in cancer.
- Cancer preventing: ‘tumour suppressor genes’, disabled in cancer.
Oncogenes and tumour suppressor genes have functions in normal cells. For example, many oncogenes are critical for normal cell growth. These genes only contribute to cancer when they are changed in a way that gives a cell a cancer-like feature.
Cancer risk factors
Many cancer-associated gene changes occur randomly within cells. Usually a single gene change in a cell is not enough to cause cancer. It is only by chance that one cell acquires enough necessary changes to develop into cancer.
There are some factors that increase a person’s risk of developing cancer:
- Older age: the risk of developing cancer increases with age. This is because over time more cancer-associated gene changes accumulate within cells.
- A family history of cancer: some people inherit a cancer-associated gene change from their parent. This gene change will be present in all their cells, meaning fewer additional changes need to occur before a cell becomes cancerous.
- Exposure to cancer-causing agents (carcinogens): some chemicals or types of radiation can cause random changes to DNA in cells. Exposure to these agents increases the risk of one cell developing all the changes necessary to cause cancer. Tobacco smoke contains many carcinogens, explaining why smokers have a higher rate of many types of cancers.
- Infection with a cancer-causing virus: some viruses carry genes that give infected cells cancer-like features.
How is cancer treated?
The goal of most anti-cancer treatments is to eliminate the cancer cells. When cancers occur as a tumour that has not spread (metastasised), they can often be removed by surgery.
When cancer cells have spread, or if a tumour cannot be safely removed by surgery, other treatments can be used to kill the cancer cells within the body.
Common treatments for cancer include:
- Radiation of the tumour and nearby tissue, which damages cancer cells enough to kill them.
- Chemotherapy, which uses medications designed to kill dividing cells. As cancer cells divide excessively, they are more susceptible to these treatments than many other cell types.
- Targeted therapies, which are designed to attack specific molecules in cancer cells, with less impact on normal cells.
Radiation and chemotherapy can kill normal cells as well as cancer cells. They often have serious side effects, such as killing infection-fighting immune cells. These side effects can lead to a person having to discontinue an anti-cancer treatment, preventing them from getting the full, most effective dose of their treatment.
Targeted therapies may have fewer side effects than chemotherapy. This means they can be used for prolonged periods to prevent cancer cell growth. Broad classes of targeted therapies include:
- Monoclonal antibodies that bind to proteins on the surface of cancer cells. This may give the cancer signals to die, or may mark the cancer cell for destruction by the immune system.
- Small molecule inhibitors, which are chemicals designed to bind to a specific protein within a cancer cell, and block its function.
- Hormonal (endocrine) therapies, used in breast and prostate cancer
Cancer resistance and relapse
Some cancer cells are not affected by anti-cancer treatments. They are called resistant (or refractory) to this treatment. In some cases, another treatment will be effective. However, some cancers develop changes that help them resist all treatments.
Relapse is the regrowth of a cancer that initially responded to treatment. Although most of the cancer cells were killed by the treatment, some were not. These cells regrow, and are often resistant to the initial treatment.
How is cancer detected?
Cancers are generally easier to treat when they are small and have not spread. Early detection of cancer is one way to prevent cancer-related deaths.
Cancer often takes months or years to develop from a single, cancerous cell. Many cancers are not diagnosed until they are large enough to prevent normal functions within the body. Cancer screening programs that are used in people known to be at risk of a certain cancer are cost-effective ways of detecting cancer early and saving lives.
In Australia, bowel cancer screening (faecal occult blood testing) for people over 50, breast cancer screening (mammograms) for women over 50, and Pap testing women for cervical cancer are widespread and effective early cancer detection tests.
Cancer Council Victoria offers detailed information about cancer treatment, and advice for people affected by cancer.
WEHI researchers are not able to provide specific medical advice specific to individuals. If you have cancer and wish to find out more information about clinical trials, please visit the Australian Cancer Trials or the Australian New Zealand Clinical Trials Registry, or consult your medical specialist.
Researchers:
Super Content:
Starting with a landmark discovery in 1988, follow the story of how Institute research has driven development of a breakthrough anti-cancer drug.
Our researchers have discovered that an existing medication could have promise in preventing breast cancer in women carrying a faulty BRCA1 gene.
Our researchers have discovered a promising strategy for treating cancers that are caused by one of the most common cancer-causing changes in cells.
In a world first, Institute scientists and collaborators have discovered a new type of anti-cancer drug that can put cancer cells into a permanent sleep, without the harmful side-effects caused by conventional cancer therapies.
Genetic sequencing shows promise for matching people with rare cancers to the right treatments, according to a new clinical trial.
Associate Professor Edwin Hawkins and his team have answered the longstanding question of how leukaemia survives chemotherapy, bringing the world closer to more effective blood cancer treatments.
Clinician scientists Associate Professor Jeanne Tie and Associate Professor Sumitra Ananda are leading trials of a blood test to guide cancer treatment after surgery.
Dr Kate Sutherland and Dr Sarah Best have revealed a unique molecular signature in the blood that could be used to detect aggressive lung cancers with a simple blood test.