Abstract
We show that mutations in the RAS oncogene sensitizes cells to drugs that target replication stress. We found that overactive RAS blocked the gene transcription of P53. These findings suggest that cancer patients with intact P53 but mutant RAS may still benefit from ATR or CKH1 inhibitors.
Original language | English |
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Place of Publication | Cancer Community |
Publisher | Nature Research |
Media of output | Online |
Publication status | Published - 8 Apr 2022 |