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Tumours often lose one of a pair of near-identical genes. They then depend entirely on the remaining copy, which a drug can block, killing only the cancer.
SMARCA4-mutant cancers depend on SMARCA2; MTAP-deleted cancers depend on PRMT5 in a methylthioadenosine-dependent manner; other paralog pairs (for example ARID1A/ARID1B, ENO1/ENO2) show the same logic. Paralog dependencies are the most systematic way to exploit tumour-suppressor loss, which is otherwise undruggable. Selective SMARCA2 degraders and MTA-cooperative PRMT5 inhibitors have reached the clinic.
Shares Drugging the 'undruggable' cancer targets, Synthetic lethality, Synthetic lethality approaches, CRISPR functional genomics.
Shares Synthetic lethality approaches, Broad Institute of MIT and Harvard, CRISPR functional genomics.
Shares Synthetic lethality, Synthetic lethality approaches, CRISPR functional genomics, The undruggable drivers.
Shares Drugging the 'undruggable' cancer targets, Broad Institute of MIT and Harvard, The Institute of Cancer Research, The undruggable drivers.
Shares Drugging the 'undruggable' cancer targets, Broad Institute of MIT and Harvard, The undruggable drivers.
Shares Drugging the 'undruggable' cancer targets, The undruggable drivers, PROTACs & molecular glues (targeted protein degradation).
Shares Synthetic lethality, Synthetic lethality approaches, Broad Institute of MIT and Harvard, CRISPR functional genomics.
Shares Drugging the 'undruggable' cancer targets, CRISPR functional genomics, The undruggable drivers.