Did you know?

Skin cancer is very common in Australia. Our “sun worshipping” attitude and outdoor lifestyle ensure that even from a young age, we receive plenty of sun. Unfortunately, the ultraviolet (UV) radiation in the sunshine can do severe damage to our skin; causing premature ageing, sunburn, and at its worst, skin cancer. Skin cancer is a disease of the body's skin cells caused mainly by cumulative exposure to UV radiation. UV radiation disrupts the cells' genes and can cause the cells to grow abnormally. If these cells are not destroyed by the body's immune system, they may develop into skin cancers. The outermost layer of the skin, the epidermis, comprises two major cell types, namely the keratinocyte and the melanocyte. The keratinocytes are the predominant cell type in the epidermis and give rise to the two most common skin cancers, the basal cell carcinoma and the squamous cell carcinoma. The melanocytes represent a small fraction of the epidermal cells but give rise to the most deadly form of skin cancer, melanoma. Basal cell carcinoma is the most common form of skin cancer, followed closely by squamous cell carcinoma. Of these, squamous cell carcinomas have the ability to spread to other sites of the body and when this happens, they are frequently fatal. Melanoma is the most deadly form of skin cancer, and can also spread to other parts of the body if not treated early. Melanoma appears as a new or existing spot, freckle or mole that changes in colour, size or shape. A melanoma usually has an irregular outline, can be more than one colour, and can grow over weeks to months, appearing anywhere on the body (including areas that aren’t exposed to the sun). Although there are many ways to prevent skin cancers, surgery to remove the cancerous cells is the main form of treatment. However, if the cancer has spread, radiotherapy and chemotherapy are the most likely methods of treatment following surgery. However, these therapies are not ideal and tend to have many side-effects. New, more selective therapeutics are desperately needed.

Skin cancer is mostly preventable. Minimise exposure in the sun, particularly between the hours of 10am and 3pm when UV levels are at their peak. Protect your skin whenever you are outdoors by wearing a hat, protective clothing, sunglasses and sunscreen.

Diamantina’s research into skin cancer

Researchers at the Diamantina Institute are investigating checkpoint mechanisms and how they become faulty in melanomas. A normal healthy adult will produce about a hundred cancerous cells every day, but why is it then that we don’t all get cancer? There are a number of checkpoints in place that prevent cancerous cells from taking hold. When cells replicate, they are scrutinised and must meet rigorous specifications before they are declared “defect free”. If not, they are destroyed.

Associate Professor Brian Gabrielli, head of the Cell Cycle Group, is investigating how the mechanisms at the checkpoints become disrupted in cancerous cells of the skin. In normal healthy cells, UV radiation will cause damage to the cell and the checkpoint will find the defect, resulting in the cells stopping to repair the damage, or if the damage is too great, destroying the cells. However, in skin cancers, the cells continue to proliferate without repairing the damage. This is because the genes for the checkpoints are often mutated in cancer and therefore do not work properly, especially in melanoma. This enables defective cells to pass through the checkpoints and keep growing, forming a cancerous lesion, like melanoma. Targeting these defective checkpoints will allow us to deliver a lethal insult to the tumour, with little toxicity to healthy tissues that have intact checkpoints.

Associate Professor Nicholas Saunders and his team in the Epithelial Pathobiology Group are studying squamous cell carcinoma. By gaining a deeper understanding of what factors regulate when a squamous cell will differentiate in normal skin, they can gain an insight into what goes wrong when a squamous cell turns cancerous. Their research has also revealed that E2F7, a transcription factor involved in the replication of skin cells, is found in higher concentrations in human cancers compared to normal healthy cells. More importantly, they found that inhibiting E2F7 sensitises cancer cells to chemotherapy, meaning that less of the toxic chemical is needed to do the same job, resulting in less of the harmful side-effects of chemotherapy. In addition, Associate Professor Saunders’ team is actively involved in the identification and preclinical validation of new therapeutic drug targets. These studies form the basis for ongoing clinical trials in patients at the Princess Alexandra Hospital with oral or cutaneous squamous cell carcinomas.

More information

For more detailed information about the research that is being done in the Cell Cycle or Epithelial Pathobiology Groups click on the links. For more information about skin cancer, we recommend you visit the the Cancer Council website or the website for the Australian Government’s National Skin Cancer Awareness Campaign.