Cancer Progression Laboratory
Mutations in important genes drives cancer. However, within a tumour, different cells can have different mutations. This genetic variation in tumours is associated with poor clinical outcomes in cancer patients, for reasons that are not clearly understood and that currently can’t be resolved.
Cells with differing mutations can interact with each other to behave more malignantly than they do on their own. They do this by producing substances that benefit each other – that promote growth, the ability to spread to other parts of the body, evade the immune system and resist treatment.
This raises the exciting possibility of a new class of therapies based on drugs that block these malignant symbiotic interactions between cancer cells. However, before such therapies can be developed, we need to understand the genes and mechanisms involved in the interactions.
Squamous cell carcinomas are cancers that arise in the outermost layer of cells in tissues that protect us from the environment, including the skin, mouth and eyes. Head and neck squamous cell carcinomas (HNSCCs) are cancers that arise in the mouth and throat and account for about 4,000 deaths in Australia each year, and 5% of cancer deaths worldwide. Treatment of advanced HNSCC usually involves surgery and radiotherapy, which do not always work, and can leave survivors disabled and disfigured. Clearly, new approaches to treating HNSCCs are needed.
Our goal is to identify the genes and cell-to-cell communication pathways that enable malignant interactions between cells in HNSCCs. This will enable ourselves and others to design and identify new drugs that block the malignant interactions and which can then be further tested in experimental models.
We sort cells from human HNSCC tumours to identify genetically distinct populations of cells that can cooperate to grow, break down tissues and provide resistance to chemotherapies. We also have mouse models that enable us to follow the progression of tumours in real time, as they transform from normal tissue to cancer, and to identify the genetically distinct populations visually. Similar models are used to examine cancers in the skin and cornea.
We sort cells from human HNSCC tumours to identify genetically distinct populations of cells that can cooperate to grow, break down tissues and provide resistance to chemotherapies. We also have mouse models that enable us to follow the progression of tumours in real time, as they transform from normal tissue to cancer, and to identify the genetically distinct populations visually. Similar models are used to examine cancers in the skin and cornea.
