Women suffering from advanced relapsed BRCA-mutated ovarian cancer could gain access to a new treatment option after European regulators waved through AstraZeneca’s Lynparza (olaparib).
The European Commission has approved the first-in-class PARP inhibitor for the maintenance treatment of adults with platinum-sensitive relapsed BRCA-mutated high-grade serous epithelial ovarian, fallopian tube, or primary peritoneal cancer, who are in complete response or partial response to platinum-based chemotherapy.
Up to 15% of women with ovarian cancer have a BRCA mutation, which is the most common cause of homologous repair deficiency. Lynparza works by exploiting tumour DNA repair pathway deficiencies to preferentially kill cancer cells.
EC clearance was based on Phase II data showing that maintenance therapy with the drug significantly prolonged progression free survival compared with placebo (11.2 months vs 4.3 months). On the safety side, the most common adverse events associated with the therapy were considered generally mild to moderate and included nausea, vomiting, fatigue and anaemia.
Welcoming its approval, John Green, Senior Lecturer, Institute of Translational Medicine, University of Liverpool and Chair of the European Network of Gynaecological Cancer Advocacy Groups, said women with a BRCA mutation “are especially at risk and there has been a significant need for new treatment options with novel modes of action”, and noted that “the development of a targeted treatment like Lynparza is an excellent example of pioneering research being translated into a treatment that has the potential to transform the lives of patients”.
Genetic fault
Meanwhile, staying with ovarian cancer, it also emerged this week that research has discovered a genetic fault that plays a key role in the development of high-grade serous ovarian cancer.
The Cancer Research UK study, published in Genome Biology, found that the gene PTEN – which helps prevent rapid cell replication – is lost in ovarian cancer cells, leading scientists to believe that its absence could trigger aggressive forms of the disease.
