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- A multi-pronged approach to targeting myeloproliferative neoplasms
- A new paradigm of machine learning-based structural variant detection
- A whole lot of junk or a treasure trove of discovery?
- Advanced imaging interrogation of pathogen induced NETosis
- Analysing the metabolic interactions in brain cancer
- Atopic dermatitis causes and treatments
- Boosting the efficacy of immunotherapy in lung cancer
- Building a cell history recorder using synthetic biology for longitudinal patient monitoring
- Characterisation of malaria parasite proteins exported into infected liver cells
- Deciphering the heterogeneity of the tissue microenvironment by multiplexed 3D imaging
- Defining the mechanisms of thymic involution and regeneration
- Delineating the molecular and cellular origins of liver cancer to identify therapeutic targets
- Developing computational methods for spatial transcriptomics data
- Developing drugs to block malaria transmission
- Developing models for prevention of hereditary ovarian cancer
- Developing statistical frameworks for analysing next generation sequencing data
- Development and mechanism of action of novel antimalarials
- Development of novel RNA sequencing protocols for gene expression analysis
- Discoveries in red blood cell production and function
- Discovering epigenetic silencing mechanisms in female stem cells
- Discovery and targeting of novel regulators of transcription
- Dissecting host cell invasion by the diarrhoeal pathogen Cryptosporidium
- Dissecting mechanisms of cytokine signalling
- Doublecortin-like kinases, drug targets in cancer and neurological disorders
- Epigenetic biomarkers of tuberculosis infection
- Epigenetics – genome wide multiplexed single-cell CUT&Tag assay development
- Exploiting cell death pathways in regulatory T cells for cancer immunotherapy
- Exploiting the cell death pathway to fight Schistosomiasis
- Finding treatments for chromatin disorders of intellectual disability
- Functional epigenomics in human B cells
- How do nutrition interventions and interruption of malaria infection influence development of immunity in sub-Saharan African children?
- Human lung protective immunity to tuberculosis
- Improving therapy in glioblastoma multiforme by activating complimentary programmed cell death pathways
- Innovating novel diagnostic tools for infectious disease control
- Integrative analysis of single cell RNAseq and ATAC-seq data
- Interaction with Toxoplasma parasites and the brain
- Interactions between tumour cells and their microenvironment in non-small cell lung cancer
- Investigation of a novel cell death protein
- Malaria: going bananas for sex
- Mapping spatial variation in gene and transcript expression across tissues
- Mechanisms of Wnt secretion and transport
- Multi-modal computational investigation of single-cell communication in metastatic cancer
- Nanoparticle delivery of antibody mRNA into cells to treat liver diseases
- Naturally acquired immune response to malaria parasites
- Organoid-based discovery of new drug combinations for bowel cancer
- Organoid-based precision medicine approaches for oral cancer
- Removal of tissue contaminations from RNA-seq data
- Reversing antimalarial resistance in human malaria parasites
- Role of glycosylation in malaria parasite infection of liver cells, red blood cells and mosquitoes
- Screening for novel genetic causes of primary immunodeficiency
- Single-cell ATAC CRISPR screening – Illuminate chromatin accessibility changes in genome wide CRISPR screens
- Spatial single-cell CRISPR screening – All in one screen: Where? Who? What?
- Statistical analysis of single-cell multi-omics data
- Structural and functional analysis of epigenetic multi-protein complexes in genome regulation
- Structural basing for Wnt acylation
- Structure, dynamics and impact of extra-chromosomal DNA in cancer
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- The cellular and molecular calculation of life and death in lymphocyte regulation
- The role of hypoxia in cell death and inflammation
- The role of ribosylation in co-ordinating cell death and inflammation
- Understanding Plasmodium falciparum invasion of red blood cells
- Understanding cellular-cross talk within a tumour microenvironment
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- Unveiling the heterogeneity of small cell lung cancer
- Using combination immunotherapy to tackle heterogeneous brain tumours
- Using intravital microscopy for immunotherapy against brain tumours
- Using nanobodies to understand malaria invasion and transmission
- Using structural biology to understand programmed cell death
- Validation and application of serological markers of previous exposure to malaria
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Cancer biology

Cancer occurs when cells develop changes that allow them to grow uncontrollably. Our cancer biology researchers are working to understand what causes these changes, how this leads to cancer, and what factors determine the success of cancer treatments. This is leading to better ways to diagnose and treat cancer.
Cancer biology research at the Institute
Our cancer researchers are discovering:
- The changes that make a normal cell become cancerous.
- The genes and proteins required for the growth and progression of cancer.
- New ways to treat cancer that target molecules essential for the cancer cell’s growth and survival.
- How to select the best treatment for a person with cancer.
How does cancer develop?
The growth of cells and tissues in the body is under tight control. This allows the body’s systems to work together. Sometimes it is important for certain cells or tissues to grow more than others. Examples of this are during the growth of a child, and the regrowth of tissue after an injury. There are many genes and proteins in cells that regulate cell growth in response to appropriate signals.
Cancer is initiated by a cell dividing uncontrollably. This is caused by changes to the genetic material (DNA) of the cell that alter the normal growth control genes and proteins. Cancer development is usually triggered after a single cell has acquired several changes that work together to drive cancer formation. Cancer cells typically contain higher-than-normal amounts of proteins that promote cancer growth. They also lack certain proteins that, in normal cells, limit growth.
Usually cancer-causing changes occur by chance (spontaneously). In some cases, cancer-causing genetic alterations are inherited from parents. Cancer-causing viruses can also introduce cancer-causing changes to cells. For example, the human papilloma virus (HPV) changes the DNA of cells in a woman’s cervix, which can lead to cervical cancer.
You can read more about the genes that are linked to cancer in our cancer page.
What makes a cancer cell?
Cancer cells have features that distinguish them from normal cells.
Normal cell |
Cancer cell |
Depends on external signals to divide |
Stimulates own division |
Limit on how many times it can divide (with the exception of stem cells) |
Can divide indefinitely |
Responds to ‘stop dividing’ signals from surrounding tissues |
Resists external ‘stop dividing’ signals |
Dies in response to internal and external signals |
Does not respond to cell death signals |
Blood vessel growth is tightly regulated into tissues |
Can stimulate growth of blood vessels into tumours |
Many processes that occur in cancer cells are also seen in normal cells. The difference between cancer cells and normal cells is how these processes are controlled. It is the improper regulation of cell division, cell death and blood vessel growth that drives cancer formation.
The features of cancer cells are caused by abnormalities in specific proteins. These abnormalities can be either an excess amount of, or a lack of, a particular protein. In some cancers, the way a protein functions, called its activity, can be changed. This is often caused by changes, called mutations, to the gene giving instructions for making the protein.
Developing treatments for cancer
Cancer is treated either by halting the growth of the cancer cells, by killing the cancer cells within the body, or by surgically removing them. If all the cells in a cancer are not completely killed or removed, there is a risk that the cancer will ‘recur’ or ‘relapse’.
Understanding how changes in genes and proteins give cells cancer-like features is leading to new treatments for cancer. Potential new anti-cancer agents are being developed that block the function of the proteins that allow cancer cell growth.
Related information:
- Medicinal chemistry: how basic cancer research can be used to develop potential new anti-cancer treatments.
- Immunotherapy: our researchers are working on an innovative form of immunotherapy that harnesses the body’s own immune cells to kill cancer cells.
- Cliinical translation: how our cancer discoveries are being translated into better treatments for patients.
Matching cancer patients to treatments
Every human cancer has developed because of unique changes to genes and proteins. Even two people’s cancers that have arisen from the same cell type can be very different at a molecular level.
These molecular differences can influence:
- How quickly the cancer grows.
- Whether, and where the cancer cells spread around the body (metastasise).
- How well the cancer responds to different treatments.
- Whether the cancer will come back (relapse) after treatment.
Our researchers are determining how people with cancer can be matched to the best treatment for their individual disease. You can read more about this on our personalised medicine page.
Researchers:
Australian cancer researchers will gain access to first-in-Australia technology through new funding from the Australian Cancer Research Foundation
A signalling molecule called interleukin-11 is a potential new target for anti-cancer therapies
Joan Heath and colleagues discovered a genetic defect that can halt cell growth and force cells into a death-evading survival state.