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Nearly all cancer drugs are found by killing fast-growing cells. Sleeping cells survive them. A screen designed around dormant cells would find a different class of drug.
Dormant disseminated tumour cells are non-cycling, so proliferation-based screens are blind to them. Induced-dormancy models exist (serum-starved and matrix-confined cells, bone-marrow-niche co-cultures, three-dimensional dormancy assays) and small screens have already flagged cardiac glycosides, autophagy inhibitors and specific metabolic dependencies. Nobody has run a million-compound campaign with dormancy-selective killing as the primary readout.
Shares DrugBank & ChEMBL, DepMap (Cancer Dependency Map), CRISPR functional genomics, Lab models that fail to predict what happens in patients.
Shares Functional (ex vivo) drug testing, Lab models that fail to predict what happens in patients, Patient-derived organoids, Dormant cells and minimal residual disease.
Shares DepMap (Cancer Dependency Map), CRISPR functional genomics, Functional (ex vivo) drug testing, Lab models that fail to predict what happens in patients.
Shares DepMap (Cancer Dependency Map), CRISPR functional genomics, Lab models that fail to predict what happens in patients, Patient-derived organoids.
Shares DepMap (Cancer Dependency Map), CRISPR functional genomics, Functional (ex vivo) drug testing, Lab models that fail to predict what happens in patients.
Shares DepMap (Cancer Dependency Map), Functional (ex vivo) drug testing, Lab models that fail to predict what happens in patients, Patient-derived organoids.
Shares CRISPR functional genomics, Functional (ex vivo) drug testing, Lab models that fail to predict what happens in patients.
Shares CRISPR functional genomics, Lab models that fail to predict what happens in patients, Patient-derived organoids.
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