A drug that targets a key gene fault could halt an aggressive womb cancer and shrink tumours, according to scientists from the Yale School of Medicine, which showed that the drug afatinib not only killed off uterine serous cancer cells after stopping their growth but also caused tumours to shrink.
The drug, a type of personalised medicine, attacks faults in the HER2 gene which lie at the heart of the cancer cells. This stops the disease in its tracks. Drugs which target HER2 are already used to treat breast cancer.
Uterine serous carcinoma is a fast-growing type of womb cancer. It is more likely than other womb cancers to come back after treatment, returning in one in two patients even if it is caught early.
Although the cancer causes less than one in 10 womb cancers, it accounts for 40% of all deaths from womb cancer – which is around 800 deaths every year in the UK.
The researchers looked at uterine serous carcinoma cell lines with normal and increased levels of the HER2 protein to see how afatinib affected the cancer. They found that the drug had a big impact on cancer cells with this gene fault, and could stop them growing and kill them. They also found that the drug shrank the size of uterine serous tumours when given to mice.
Afatinib works by targeting receptors that respond to growth signals. Cancers with high levels of the HER2 protein have too many of these receptors, allowing them to grow out of control. The drug is an example of personalised or tailored treatment, which works by specifically targeting the faulty genes and molecules in an individual’s cancer. Afatinib is being tested in clinical trials for a number of cancers including bowel cancer and certain types of lung and breast cancer.