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Chromosomally unstable, often whole-genome-doubled tumours survive constant chromosome mistakes by depending on the motor protein KIF18A, which diploid cells do not need. Blocking it kills unstable cancer cells while sparing normal ones; inhibitors are in early trials in ovarian and other cancers.
Chromosomally unstable, often whole-genome-doubled tumours depend on the kinesin KIF18A for mitotic fidelity, whereas diploid cells do not. KIF18A inhibitors are in early trials in ovarian and other CIN-high cancers. The proposal is to use CIN and whole-genome doubling, measured from routine sequencing, as the selection biomarker and to test KIF18A inhibition specifically after platinum resistance, when instability is highest.
Shares Synthetic lethality, Synthetic lethality approaches, CRISPR functional genomics, The undruggable drivers.
Shares Synthetic lethality, Synthetic lethality approaches, CRISPR functional genomics, The undruggable drivers.
Shares Synthetic lethality, Synthetic lethality approaches, CRISPR functional genomics.
Shares Synthetic lethality, Synthetic lethality approaches, CRISPR functional genomics, The undruggable drivers.
Shares Synthetic lethality approaches, CRISPR functional genomics.
Shares Synthetic lethality, Synthetic lethality approaches, CRISPR functional genomics, The undruggable drivers.
Shares Synthetic lethality approaches, CRISPR functional genomics.
Shares Synthetic lethality approaches, Ovarian cancer, Triple-negative breast cancer (TNBC).