Leukaemia is a cancer of the blood or bone marrow involving abnormal proliferation of blood cells.
It is projected that there are over 3,500 new cases of leukaemia diagnosed in Australia every year. (Source – Australian Institute of Health and Welfare)
Acute Lymphoblastic Leukaemia (ALL) is one of the most deadly and most common types of leukaemia affecting children aged 0 to 14 years and may also occur in adults.
Hunter researchers have identified a molecule that is abnormally expressed in leukaemia cells and not in normal bone marrow or white blood cells, making it a good target for new therapies. FAT1 cadherin is a molecule that helps to control cell growth and hence when it is dysregulated, cancer can occur. Current research aims to develop complimentary molecules that can target FAT1 and improve the outcomes of patients with leukaemia.
Another type of leukaemia, Acute myeloid leukaemia (AML), is a rapidly progressing blood cancer predominantly affecting older adults, and has the lowest survival rate of all the leukaemias at 24% for a 5 year survival (Source – Australian Cancer Council).
A molecule called BAALC (brain and acute leukaemia cytoplasmic) has been shown by Hunter researchers to be overexpressed in leukaemia and breast cancer cells. BAALC may also be used as a predictive marker in patients to determine which drugs may be effective in their treatment and how severe their disease may become. A new inhibitory molecule has been developed by Hunter researchers which targets the site and can kill leukaemia cells resistant to currently used chemotherapeutics, whilst sparing normal cells.
"If scientists can identify proteins that are different in cancerous cells, or in drug-resistant cells, then we can design drugs to target those differences – drugs that will specifically kill cancerous cells but not normal cells" explains researcher Nikki Verrills at the University of Newcastle.
Dr Verrills and her team have been working on another molecule that is altered in leukaemia, known as phosphatase 2A, or PP2A. Hunter researchers have found that PP2A is ‘turned off’ in cancer cells and if they can switch it back on, they may be able to get cancer cells to stop growing on their own, without harming normal cells of the body.
