Tamoxifen, developed more than 30 years ago to treat breast cancer, prevents oestrogen from stimulating the growth of breast cancer cells. It is prescribed for women who are ER positive. That means that oestrogen receptors (ER) have been found on their breast cancer cells. The oestrogen receptor is the part of the breast cancer cell that oestrogen attaches itself to, triggering a chain of events which can lead to the cell growing and dividing in an uncontrolled manner and forming a tumour.

Work from Professor Isacke's team, funded by AICR and Breakthrough Breast Cancer, focuses on situations where, even when oestrogen is not present, the oestrogen receptor can become activated.

In their current paper, published in leading cancer journal Oncogene, they show that when a protein called RET is switched on, it can activate the oestrogen receptor in the absence of any oestrogen.

To confirm their findings from the laboratory, they took tissue samples from oestrogen positive breast cancer patients and found that they had increased levels of RET. They went on to show that reducing the levels of RET actually makes the breast cancer cells more sensitive to tamoxifen and more likely to die.

Speaking from the Breakthrough Breast Cancer Research Centre at the ICR, in London, where she leads the Molecular Cell Biology Team Professor Isacke said: "We are very excited by these findings. Our challenge now is to work out how RET activates the oestrogen receptor so that we can develop new treatments for tamoxifen-resistant breast cancers"

SOURCE The Institute of Cancer Research