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As approximately 96% of patients with high-grade serous ovarian cancer harbor the tumor suppressor p53 gene, WEE1 inhibitors have demonstrated evidence of chemopotentiation in p53-deficient tumors.

One of the papers I highlighted in my talk looked at p53 mutated patients using AZD1775 with carboplatin in platinum-refractory patients. In the face of a p53 mutation and the WEE1 pathway that it followed, they had a 46% response rate. Therefore, that might be a very interesting drug, simply because also close to 100% of all patients with ovarian cancer with high-grade serous tumors are going to carry p53 mutations .

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