Phenotypic characterization of the novel, non‑hotspot oncogenic KRAS mutants E31D and E63K

KRAS proto‑oncogene, GTPase (KRAS) functions as a molecular switch at the apex of multiple signaling pathways controlling cell proliferation, differentiation, migration, and survival. Canonical KRAS mutants, such as those in codons 12 and 13, produce constitutively active oncoproteins that short‑circuit epidermal growth factor receptor (EGFR)‑initiated signaling, resulting in dysregulated downstream effectors associated with cellular transformation.