Scientists at Cancer Research UK say they have discovered the molecular basis for tamoxifen response in breast cancer cells - and the reason why some women can develop resistance to the treatment.

In a study published in Nature, researchers at the charity’s Cambridge Research Institute say that they have discovered for the first time the mechanism by which tamoxifen operates. It switches off a breast cancer gene ErbB2 via a protein called Pax2, which acts as a ‘switch’ to keep ErbB2 switched off.

Tamoxifen resistance occurs when ErbB2 remains switched on, CR UK says. Previously it was known that tamoxifen worked by blocking oestrogen from causing unchecked cell growth in breast cancer by switching certain genes on but the mechanism by which this occurred was unknown.

Lead author Jason Carroll writes that previously our understanding of why resistance to the treatment occured “could be compared with trying to fix a broken car without knowing how the engine worked. Now we understand how all the engine parts operate and we can try to think about ways to make repairs”.

Sir David Lane, CR UK’s chief scientist said the charity’s early clinical trials of tamoxifen helped “transform the way that women were treated for early breast cancer saving tens of thousands of lives, and this work is yet another step forward”. He added that the drug has been “a huge success story” and “understanding why it occasionally stops working is really important because it allows us to identify new targets for drug development and who will need such treatments.”