Time-to-event end points considered latencies following initial diagnosis and were analyzed using the Kaplan-Meier method and compared using the log-rank test. The median follow-up time with associated CI was calculated using the reverse Kaplan-Meier method. 22įisher exact tests were used to assess the associations between categorical variables, and Wilcoxon rank-sum tests were used to assess associations between continuous variables between the treatment cohorts. Radiotherapy (RT) treatment details have been previously reported. 21 Patients who had local therapy to the primary and all metastatic lesions were considered to have received comprehensive LCT patients receiving local therapy to some but not all of the sites were considered to have received subcomprehensive LCT patients not treated with local therapy to any site were considered to have received no LCT. 20 The radiographic response to initial systemic therapy was assessed using RECIST 1.1 criteria. 4 Intrathoracic disease stage was assigned using the American Joint Committee on Cancer 8th Edition staging system. 4 Intrathoracic nodal disease was counted as a single site, regardless of the number of nodes involved, consistent with categorizations previously described. Discrete metastatic foci within a single organ were counted as separate sites. 16 We used the MD Anderson Cancer Center GEMINI database, a prospectively collected database including tumor molecular profiles. Cohort selection has been previously described. 18, 19 Therefore, we aimed to understand patterns of molecular alterations in patients presenting with synchronous oligometastatic NSCLC, and to identify associations with outcomes.Īfter approval by the University of Texas MD Anderson Cancer Center Institutional Review Board (PA16-0061), we identified patients presenting to our institution between January 1, 2000, and December 31, 2017, with stage IV NSCLC and ≤ 3 synchronous (defined as present at the time of initial diagnosis) metastatic lesions. 16, 17 Furthermore, such investigations have been limited to alterations of EGFR without broader consideration of other mutations, for which novel agents are likely to be approved in the coming years. 14, 15 Despite the parallel efforts of investigation into cLCT and development of targeted therapies in stage IV disease, few studies have characterized the outcomes of patients with NSCLC receiving cLCT on the basis of genetic alterations. 11- 13 Tyrosine kinase inhibitors (TKIs) targeting these mutations and their downstream effectors have enabled long-term survival. Testing for actionable mutations/alterations of EGFR, ALK, ROS1, MET, BRAF, and NTRK has been increasingly performed over the past two decades. Current guidelines recommend testing for molecular biomarkers in NSCLC to guide therapy. As novel molecularly targeted therapies emerge, treatment combining comprehensive LCT with targeted therapy in selected patients warrants further investigation.Ĭoncurrently, there has been growing interest in the development of molecularly targeted agents that can be used in lieu of cytotoxic chemotherapy for patients with advanced disease. These findings suggest that comprehensive LCT, when combined with molecularly targeted therapy for EGFR-mutated patients, may enable long-term survival. We also demonstrate that patients with EGFR mutations who received both EGFR-targeted therapy and comprehensive LCT had significantly longer overall survival than those with EGFR wild-type tumors (98 v 29 months). In this cohort study of 194 patients, we provide evidence that EGFR mutations are associated with longer overall survival (OS) and that STK11 mutations are associated with shorter progression-free survival. This retrospective cohort study aimed to identify genomic associations with outcomes for these patients. Local consolidative therapy (LCT) for patients with synchronous oligometastatic non–small-cell lung cancer is an evolving treatment strategy, but outcomes following LCT stratified by genetic mutations have not been reported.
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