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Breakthrough drug to stop aggressive womb cancer growth

Research recently published in the British Journal of Cancer has revealed that a new drug which has been developed to target a key gene fault in women could help halt an aggressive form of uterine cancer.

A team of scientists from the Division of Gynaecologic Oncology at Yale School of Medicine showed that the drug known as afatinib aids womb cancer patients by not only killing off uterine serous cancer cells after stopping their growth but also caused tumours to shrink significantly.

The drug, which is expected to be offered as a type of tailored medication, attacks faults in the HER2 gene which often lie at the heart of womb cancer cells. By attacking this gene fault, the drug manages to stop the cancer in its tracks, as the gene is what controls how the cancer spreads.

Drugs which treat the HER2 gene fault are currently already being used as treatment for breast cancer, which should mean that once approved for the use of treating womb cancer, it should be readily available for patients with a targeted treatment plan.

Nell Barrie, the senior science information manager at Cancer Research UK said: “Targeted treatments like afatinib offer an opportunity to home in on the faults at the heart of each cancer. The findings of this research still need to be proven in people, but this research suggests that afatinib could be an effective treatment in treating this rare but aggressive type of cancer.”

The HER2 gene is found in patients who have a form of womb cancer known as uterine serous carcinoma. This is a fast-growing type of cancer and more likely to come back after the patient has received treatment.

The research team analysed uterine serous carcinoma cells lines with normal levels of the HER2 gene protein, and those with increased levels to see how the drug afatinib affected the cancer. The drug was found to have a big impact on cancer cells which had increased levels of HER2 and could help stop them from growing, before destroying them altogether.

 

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