Article
Keap1 mutation renders lung adenocarcinomas dependent on Slc33a1.
Nature cancer - 1 Jun 2020
Romero Rodrigo, Sánchez-Rivera Francisco J, Westcott Peter M K, Mercer Kim L, Bhutkar Arjun, Muir Alexander, González Robles Tania J, Lamboy Rodríguez Swanny, Liao Laura Z, Ng Sheng Rong, Li Leanne, Colón Caterina I, Naranjo Santiago, Beytagh Mary Clare, Lewis Caroline A, Hsu Peggy P, Bronson Roderick T, Vander Heiden Matthew G, Jacks Tyler
Abstract excerpt
Approximately 20-30% of human lung adenocarcinomas (LUAD) harbor loss-of-function (LOF) mutations in Kelch-like ECH Associated-Protein 1 (KEAP1), which lead to hyperactivation of the nuclear factor, erythroid 2-like 2 (NRF2) antioxidant pathway and correlate with poor prognosis1-3. We previously showed that Keap1 mutation accelerates KRAS-driven LUAD and produces a marked dependency on glutaminolysis4. To extend...
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