The emphathy breast
In 2007, more than 12,500 Australian women were diagnosed with breast cancer. This does not include the 7,000 women alive today who were diagnosed with cancer that has spread from the breast to other parts of the body (known as secondary, advanced or metastatic breast cancer). Only 40% of these women will survive more than five years after diagnosis. This is almost half the chance of survival for women diagnosed with primary breast cancer.
Once breast cancer has spread to other parts of the body, (most commonly, the bones, brain, liver or lungs), it usually cannot be cured. Many women are living with chronic disease as current treatments only relieve symptoms and control further spread of the disease.
Cells in the secondary tumour of these women have a distinctly different history from cells in the breast tumour. These cells have acquired the ability to invade blood vessels or lymphatic vessels as well as the ability to move and establish cancer in other tissues. The cells may also be drug resistant and able to survive attacks by the immune system. These differences are the reason why secondary breast cancer can escape treatments that would normally cure primary breast cancer.
“The increased motility, invasiveness and adaptability of the cells that cause secondary breast cancer may be explained by epithelial mesenchymal plasticity (EMP). EMP is a term used to describe a collection of molecular and cellular processes that allow cells to fluctuate between a structured, stationary, ‘epithelial’ state and a motile, less controlled, ‘mesenchymal’ state,” said Professor Erik Thompson, founder of the EMPathy Network.
Professor Thompson and the EMPathy team are working to identify specific changes in the molecular characteristics that affect the shape and behaviour of the cells that form secondary breast cancer. The researchers will use these differences to design an effective method to detect these cellular changes early and to develop new drugs that will prevent secondary breast cancer from occurring.