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The ICR responds to the FDA approval of olaparib for women with BRCA-mutant advanced breast cancer

Institute of Cancer Research News Jan 17, 2018

The Institute of Cancer Research (ICR), London, strongly welcomes the news that olaparib has been approved by the US Food and Drug Administration (FDA) for patients with advanced breast cancer.

Science carried out at the ICR underpinned the development of PARP inhibitors, such as olaparib, for women with BRCA-mutant breast and ovarian cancer.

Professor Andrew Tutt, director of the Breast Cancer Now Research Centre at the ICR, was part of the early laboratory research behind PARP inhibitors in patients with BRCA mutations, and led some of the early clinical trials of olaparib. He said:

“We are delighted that the FDA has approved olaparib for advanced breast cancer in women who have inherited BRCA1 or BRCA2 mutations. This is excellent news for women with this uncommon but important genetic form of breast cancer many of whom took part in the clinical trials.”

“The first steps in this journey were made in Alan Ashworth’s lab at the ICR, funded by Breast Cancer Now and Cancer Research UK. The discoveries made then drove the development of clinical trials in breast cancer, both at the ICR and The Royal Marsden NHS Foundation Trust, and with our many international genetic oncology colleagues.”

Professor Chris Lord, deputy director of the Breast Cancer Now Research Centre, at the ICR, said:

“This drug is a perfect example of how understanding a patient’s genetics and the biology of their tumor can be used to target its weaknesses and personalize treatment. Olaparib will now provide thousands of women in the US with a treatment that acts directly against their inherited genetic mutation.”

“We are very proud to have played a part in the discovery and development of this drug and now eagerly await decisions by the European Medicines Agency, and ultimately NICE, which we hope will make olaparib available to women with BRCA mutant breast cancer in the UK as soon as possible.”

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