Objectives Mutation analysis by massive parallel sequencing (MPS) is routinely performed in the clinical management of lung cancer in Sweden. We describe the clinical and mutational profiles of lung cancer patients subjected to the first 1.5 years of treatment predictive MPS testing in an autonomous regional health care region. Methods Tumors from all patients with lung cancer who had an MPS test from January 2015 to June 2016 in the Skåne health care region in Sweden (1.3 million citizens) were included. Six hundred eleven tumors from 599 patients were profiled using targeted sequencing with a 26-gene exon-focused panel. Data on disease patterns and characteristics of the patients subjected to testing were assembled, and correlations between mutational profiles and clinical features were analyzed. Results MPS with the 26-gene panel revealed alterations in 92% of the 611 lung tumors, with the most frequent mutations detected in the nontargetable genes TP53 (62%) and KRAS (37%). Neither KRAS nor TP53 mutations were associated with disease pattern, chemotherapy response, progression-free survival, or overall survival in advanced-stage disease treated with platinum-based doublet chemotherapy as a first-line treatment. Among targetable genes, EGFR driver mutations were detected in 10% of the tumors, and BRAF p.V600 variants in 2.3%. For the 71 never smokers (12%), targetable alterations ( EGFR mutations, BRAF p.V600, MET exon 14 skipping, or ALK/ROS1 rearrangement) were detected in 59% of the tumors. Conclusion Although the increasing importance of MPS as a predictor of response to targeted therapies is indisputable, its role in prognostics or as a predictor of clinical course in nontargetable advanced stage lung cancer requires further investigation.

Background: We set up our treatment protocol performing upfront surgery for non-bulky, single-station clinical N2 (cN2a) patients. Method: Between 2012 and 2016, 129 patients underwent upfront surgery for cN2a disease diagnosed on CT and PET-CT findings. 85 patients underwent preoperative invasive mediastinal staging (IMS group), whereas, in 44, IMS was not performed (Non-IMS group). Survivals were compared with log-rank test. Subgroup analysis for pN2-3 is performed to identify prognostic factors using Cox-regression. Result: Pathologic N stages were pN0-1 in 26 patients (20%: 18 IMS, 8 non-IMS), pN2a in 51 (40%: 33 IMS, 18 non-IMS), pN2b in 47 (36%: 29 IMS, 18 non-IMS) and pN3 in 5 (4%: all IMS). The overall 5-year survival was 55.4% with no difference between groups (p¼0.19). In pN2-3 patients, 5-year survival was 51.0% and IMS group was better (p¼0.05). In a Cox's regression, non-IMS (HR 1.89, p¼0.04), no adjuvant chemotherapy (HR 3.55, p<0.001), extensive burden of metastatic lymph nodes (number of metastatic LN13, HR 3.32, p¼0.002) were independent risk factors for survival. Conclusion: We found significant number of cN2a patients were pN2b-3 even after IMS, but surgery resulted in reasonable survival. This suggests upfront surgery for cN2a disease is a valid option if preoperative IMS and adjuvant chemotherapy are warranted.