482P Tumor and plasma mRNA profiling of KRAS-related genes potentially associated with outcome in KRAS G12C-mutated non-small cell lung cancer

Results: WES identified recurrent mutations in TP53, EGFR, CDH7, LRRIQ3, CSMD1, EPHA3, GIGYF2, and TARP.TARP copy-number gain was enriched in LUAD-TB vs. controls (37.5% vs. 5%; q=0.02).Enriched pathways included cell adhesion (q=0.03) and CNS development (q=0.04).IHC (n=56) validated high expression of CDH7 (28%), EPHA3 (22%), GIGYF2 (31%), and TARP (19%).TARP protein correlated with copy-number gain (=0.72,p<0.001).PD-L1 positivity (30%) did not correlate with TMB (p=0.55) or EGFR status (p=0.47).Conclusions: LUAD arising in the setting of active TB exhibits a distinct infectionrelated genomic signature, characterized by TARP amplification and dysregulation of cell adhesion pathways.The lack of correlation between PD-L1 and TMB suggests unique immune escape mechanisms in this subgroup.TARP emerges as a potential biomarker or therapeutic target.These findings underscore the necessity for tailored molecular stratification for patients with specific comorbidities in TB-endemic regions.