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Abstract WEE1 phosphorylates and inhibits the activity of cyclin-dependent kinases to prevent mitotic entry and establish a G2 DNA damage checkpoint1,2,3. Consequently, WEE1 inhibitors have been developed to be synthetically lethal in TP53-mutated tumours that become reliant on this WEE1-mediated checkpoint, and such inhibitors are undergoing clinical trials.
Abstract For all drugs, effective target engagement requires sufficient intracellular concentrations of drug to be reached, but whether tumour heterogeneity impacts drug distribution and efficacy is poorly studied. Poly (ADP-ribose) polymerase (PARP) inhibitors have transformed treatment opportunities for women with high-grade serous ovarian carcinoma, but resistance remains a clinical hurdle in this highly heterogeneous tumour type.
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