Truncation of the PTV for Minimization of Risk of Chest Wall Toxicity in Patients Receiving SBRT for Stage I NSCLC

Abstract

response heterogeneity between the primary and metastasis tumor increased significantly as H r1 (13.3%) ＜ H r2 (25.6%)＜ H r3 (46.1%)＜ H r4 (53.5%) ＜H r5 (56.9%). We identified EGFR T790M as the most common mechanism of acquired resistance (63.6%). No pre-EGFR-TKI tumor had a preexisting T790M mutation. The capability of response heterogeneity parameter to predict T790M was shown by the ROC. Hr4 and Hr3 predicted T790M mutation (AUCZ0.826and 0.783, respectively) more accurately than other parameters did. PFS and OS was significantly shorter in patients with higher response heterogeneity between primary and metastasis (P Z 0.006). Compared to T790M-positive tumors, T790Mnegative tumors showed relatively higher response heterogeneity between the primary and metastasis tumor and shorter survival, suggesting T790Mnegative patients as a potential candidate for early topical therapy. Conclusion: The therapeutic response of TKI showed significance difference between primary and metastasis tumors in advanced NSCLC. The gap increased month-by-month. Higher intra-tumor response heterogeneity showed correlation with T790M-negative and poor outcome. Dynamic radiogenomics analysis will provide a systems-level understanding of underlying heterogeneous cellular and molecular processes of acquired resistance molecular mechanisms.