Researchers have identified a new protein involved in the development of drug resistance in breast cancer which could be a target for new treatments, they report today in the journal Nature Medicine.
In a mouse model of breast cancer, blocking production of the protein using genetic techniques caused tumours to shrink. The scientists are now looking for new drugs which could achieve a similar effect.
Breast cancer is the most common cancer in the UK, affecting about 46,000 women each year. More than two thirds of breast tumours contain oestrogen receptors, meaning that they require the hormone oestrogen to grow and they can be treated with anti-oestrogen drugs such as tamoxifen. However, many patients develop resistance to these treatments so that the drugs eventually cease to be effective.
In today's study, researchers from Imperial College London found that blocking a protein called LMTK3 in human cancer cells that were resistant to tamoxifen made the cells more responsive to the drug. In a mouse model of the disease, using genetic techniques to block the production of LMTK3 led to a significant decrease in the size of breast tumours.
The researchers also measured levels of LMTK3 in tissue samples taken from women with breast cancer. They found that women who had higher levels of LMTK3 in their tumours tended to live less long and were less likely to respond to hormone therapy. In addition, they found that particular mutations in the gene coding for LMTK3 also correlated with how long a patient would survive.
"Anti-oestrogen drugs have been very successful at allowing women with breast cancer to live longer, but resistance to these drugs is a common problem," said Professor Justin Stebbing, from the Department of Surgery and Cancer at Imperial College London, the study's senior author. "Our results suggest that the action of LMTK3 on the oestrogen receptor has a crucial role in the development of drug re
|Contact: Sam Wong|
Imperial College London