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Abstract Although poly(ADP-ribose) polymerase inhibitors (PARPi) show promise for treating homologous recombination-deficient cancers, the observed PARPi hypersensitivity in additional genetic contexts expands their potential use in precision oncology. Yet, the DNA lesions driving PARPi-induced cytotoxicity remain poorly defined. Here we uncover distinct replication-fork lesions in specific genomic regions as key determinants of PARPi cytotoxicity.
Communication Dr. S. Denise Field Corresponding Author E-mail address: denise.field@pfizer.com Pfizer Worldwide Research and Development, 1 Portland St, Cambridge, MA, 02139 USA These authors contributed equally to this work. Search for more papers by this author Abstract One and only one : The degradation susceptibility of serine hydrolases was assessed by using a probe that contained a fluorophosphonate warhead and a cereblon‐binding pomalidomide.
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