Few things strike fear into people more than the word cancer, and with good reason. While improvements in cancer therapy and advances in palliative care mean that the illness does not always lead to inevitable and painful death as it once did, approximately one in three of us will get some form of cancer in our lifetime.
Cancer accounted for about three in ten deaths (over 42,000) in Australia last year. It was the second most common cause of death after cardiovascular disease. Aside from the obvious personal cost, cancer is expensive, with direct costs to our national health system running at $3.8 billion a year.
The US National Cancer Institute defines cancer as a disease in which abnormal cells divide without control and are able to invade other tissues.
Our bodies contain over 200 different types of cell, the basic units of life. Each of these has specific functions and is organised into the various organs such as the lungs, liver, skin, and brain. To keep these organs functioning, cells grow and divide to replace other cells as they age and die.
The exquisite balance between cell growth and death is normally kept under tight control by an incredibly complex genetic network. Mutations in the DNA of genes controlling the network can disrupt this balance, causing an accumulation of excess cells, which forms a tumour.
If a tumour forms in an essential organ, such as the liver or lungs, it may eventually grow large enough to compromise organ function and kill us. But some of the most common cancers occur in organs that aren’t necessary to keep us alive, such as breasts and prostate. Here, the real problems usually arise when cells from the primary tumour spread (metastasise) to form secondary tumours in essential organs.
It’s staggering to think that a mutation in any one of the 100 trillion or so cells in our body is all it takes to initiate a tumour. Cancer-causing mutations can be inherited, or induced by infection with bacteria or viruses (HPV and HIV), or environmental factors, such as smoking, asbestos and radiation.
But most mutations probably occur as the result of unrepaired DNA damage that is a consequence of normal cell metabolism.
Complexity is one of the most challenging aspects of understanding cancer and developing therapies. At the molecular level, this complexity can be reduced to a relatively small number of underlying principles known as the hallmarks of cancer. But the more we learn about cancer at the genetic level, the more we understand that each person’s disease is unique.
In other words, cancer is not a single disease. Over 100 different types of cancer have been described using anatomical classifications – that is, by the organ or cell type in which they originate (such as prostate cancer, bowel cancer, breast cancer, skin cancer and lung cancer). But common molecular features (such as a particular genetic signature) are emerging as a much more powerful way to determine appropriate treatment.
This paradigm shift in treatment is being driven by large-scale gene sequencing and functional genomics projects, which are giving us unprecedented insight into cancer at the genetic and molecular level. Australia is at the forefront of this effort, particularly in pancreatic and ovarian cancer genomics.
By far the strongest risk factor for cancer is age. Put simply, the older you get, the better your odds of getting cancer. A long list of genetic and environmental risk factors have been identified for various cancer types, but many of these have relatively moderate effects.