NSCLC is a heterogeneous disease, with multiple oncogenic mutations (e.g. KRAS, LKB1). NSCLC patients have a variety of clinical courses, which are partly due to differences in co-occurring molecular events [1]. Since both KRAS mutation and LKB1 loss have an impact on cellular metabolism, it is fundamental to discern the metabolic effects induced by single genetic events from those induced by their co-occurrence, for novel therapeutic interventions.
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