February 4, 2015
The Westmead Millennium Institute for Medical Research hosts the largest team of cancer researchers in New South Wales. This multi-disciplinary team investigates a wide range of cancers and in the last 12 months has published several significant findings.
Understanding why ovarian cancer becomes resistant to chemotherapy was the focus of research published in the journal Oncogene by a team led by WMI’s Dr Ying Lei and Professor Anna DeFazio and including Associate Professor Henderson, Dr Catherine Emmanuel and Professor Paul Harnett.
The team searched for genes that could potentially be targeted to sensitise or re-sensitise ovarian cancer cells to chemotherapy.
“Primary and acquired chemotherapy resistance remains a major challenge in the treatment of epithelial ovarian cancer and there are currently few targeted treatments that can improve patient survival,” said Dr Lei.
“We discovered a new gene – ANKRD1 – not previously described in ovarian cancer and found that higher expression levels of this gene are associated with poor patient survival.”
An important discovery in the battle against leukaemia was the result of research by Associate Professor Linda Bendall, published in the journal Cancer Research.
Her research looks at how using drugs to inhibit the enzyme sphingosine kinase 2 (SK2) induces death in acute lyphoblastic leukaemia cells and reduces progression of the disease.
“We found that enzyme SK2 is required for the optimal development of leukaemia and if we delete or inhibit the enzyme the leukaemia cells die,” said Associate Professor Bendall.
“Of particular interest is that this approach works in synergy with some agents that are used to treat leukaemia – in particular some of the targeted therapies that have just entered use, such as the TKI Gleevec – and others currently in development.”
Cancer Cell Biology
WMI Associate Professor Beric Henderson has been researching the role of actin polymerisation in a cell.
His paper, published in the journal BBA Molecular Cell Research, described the results of a four-year study using innovative techniques to view live cells and the movement of actin into the nucleus of those cells.
“We discovered that in response to DNA damage or cell cycle arrest the actin quickly shifted into the nucleus, along with two co-factors, to form actin filaments,” said Associate Professor Henderson.
“This response might one day lead to a better understanding of the mechanisms by which chemotherapeutics block the replication of DNA in cancer cells.”