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Oncogenic KRas mutations are present in about 30% of all human cancers and in more than 90% of pancreatic cancers. KRas-driven cancers have been largely resistant to therapeutic intervention and KRas itself has been considered undruggable. However, two recent studies have uncovered what may be an Achilles’ heel for cancer cells harboring activating KRAS mutations [1, 2]. These studies exploit a bypass of a late G1 glutamine (Gln)-dependent cell cycle checkpoint in cancer cells with KRAS mutations [3]. Upon Gln deprivation, KRas-driven cancer cells enter S-phase and arrest due to insufficient nucleotide biosynthesis [4]. The S-phase arrested cells are then vulnerable to the cytotoxic drugs capecitabine, paclitaxel, and rapamycin [1, 2]. Thus, Gln deprivation creates a “synthetic lethality” for capecitabine, paclitaxel, and rapamycin in KRas-driven cancer cells.

Synthetic lethality in KRas-driven cancer cells created by glutamine deprivation