Did you know?

One in two men and one in three women will be diagnosed with cancer before the age of 85 years.

The face of cancer is changing. Years ago, a diagnosis of cancer was often an equivalent to a death sentence. However, thanks to modern medical research driving advances in diagnostics and treatments, survival rates for cancers are the highest they have ever been.

One in two men and one in three women will be diagnosed with cancer before the age of 85 years. A sobering fact, and one that scientists are working very hard to do something about. Thanks to breakthroughs in medical research, diseases like breast cancer have a significantly higher survival rate. Due to improved treatments and detection methods, the survival rate of breast cancer has increased 18% in Australia over the past ten years.

Although scientists still don’t have a magic silver bullet for curing cancer, they are exploring the mechanisms of cancer in order to gain a deeper understanding of why a cell will turn cancerous in the first place, and how we can interrupt the cycle before it develops further. These findings will lead to new therapies and detection methods.

What is Cancer?

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. Firstly, when cells replicate, they are scrutinised and must meet rigorous specifications before they are declared “defect free”. If not, they are destroyed. Secondly, the immune system has a surveillance system that searches and destroys cells that have defects. When you consider that humans are made up of approximately 50 trillion cells, and that your cells are constantly replicating and dividing, it’s surprising that more things don’t go wrong!

In order to understand what happens when a cell becomes cancerous, it is important to understand two important characteristics of normal healthy cells. Cells will naturally replicate and divide at a controlled rate. This rate is controlled by certain genes within a cell. There are some genes that increase the rate of replication, and some that slow down how often a cell replicates. This very careful and finely-tuned balance can be likened to an accelerator and brake system in a car. In order to keep the car going at a constant rate, you can either accelerate to speed up, or break to slow down.

The other key characteristic of normal cells is that they have the ability to self-destruct, also known as apoptosis. They do this when the cells are old, damaged or if they are somehow causing harm to the rest of the body.

It takes many ‘attacks’ by a combination of environmental triggers and defective genes for a cell to become cancerous. When a cell does reach that point, it no longer divides at a controlled rate, but instead replicates furiously, resulting in a mass of cells, known as a tumour. The genes responsible for controlling the rate of replication have been damaged: It’s as though the accelerator is pressed all the way down to the floor, or that the break isn’t being used, resulting in the car driving very fast and out of control. Cancer cells also become ‘immortalised’, no longer having the ability to self-destruct. This powerful combination enables cancerous cells to survive, and to survive well. They also have the ability to hide from the immune system, which would normally seek and destroy these rogue cells. The tumour may eventually send chemical signals to nearby blood vessels, inviting them to infiltrate the tumour with blood vessels. Once this occurs, it can grow rapidly from the nutrients received from the bloodstream and now also has the ability to send cancerous cells off to other parts of the body via the bloodstream. This is known as metastasis.

Diamantina's research into cancer

There are many places along this pathway that scientists are trying to intervene to stop a cell becoming cancerous. 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, ultraviolet 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, to be destroyed. 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.

Another researcher at the Diamantina Institute is using molecular profiling techniques to investigate if a cancer is likely to spread, or metastasise. This is often a fatal complication. Associate Professor Nicholas Saunders said his team in the Epithelial Pathobiology Group had been working on a relatively rare cancer that most commonly affected children and young adults, called osteosarcoma. Their research showed that they could predict with 93% accuracy if a patient would go on to develop metastatic disease. They found that one gene was able to predict what is known as “metastatic potential” and so they are now performing an in-depth analysis of this gene since they believe it may be responsible for controlling metastasis.

By investigating the molecular biology of individual cancers and identifying exactly where and when a cell turns cancerous, researchers will be able to find targets and develop specific treatments against it. This kind of therapy would prove much more effective and have significantly less side-effects than today’s treatment of chemotherapy, which targets rapidly proliferating cells – both cancerous and non-cancerous – resulting in the debilitating side-effects that are all too familiar to many cancer patients.

We already know that the human papillomavirus causes cervical cancer but it has long been wondered what other cancers might be caused by this virus. Associate Professor Nigel McMillan and his team in the Molecular Virology Group have found that the human papillomavirus is present in the pre-cancerous areas of the prostate suggesting that this virus may play a role in some or all types of prostate cancer. This work has important implications for the treatment of this disease and we are ideally placed to investigate potential vaccines that might prevent men getting prostate cancer.

By understanding the underlying biology of cancer, scientists are getting a step closer to developing new therapies and preventative measures like vaccines. The tide is certainly turning on the battle against cancer.

You can help support our scientists in their quest for finding a cure for cancer. Please support us today.