Year: 2015
Type: article
Abstract: A. Foster 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
Source: Oncoscience
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W2415181728