The RAS-RAL axis in cancer: evidence for mutation-specific selectivity in non-small cell lung cancer

摘要: Activating RAS mutations are common in human tumors. These often markers for resistance to therapy and subsequent poor prognosis. So far, targeting the RAF-MEK-ERK PI3K-AKT signaling pathways downstream of is only promising approach treatment cancer patients harboring mutations. RAL GTPase, another effector RAS, also considered as a therapeutic option RAS-mutant cancers. The GTPase family comprises RALA RALB, which can have either divergent or similar functions different tumor models. Recent studies on non-small cell lung (NSCLC) showed that selectively activate specific pathways. This observation requires broader validation other tissue types, but if true, will provide new by effectors according type mutation. It suggests inhibition be an important strategy tumors glycine cysteine (G12C) glycien valine (G12V) mutations, commonly found NSCLC pancreatic cancer.