Objective: We previously identified amplified fibroblast growth factor 1 (FGFR1) as a therapeutic target for small molecule inhibitor (SMI) therapy in squamous cell lung cancer (L-SCC), resulting in currently running clinical trials treating patients with stage III disease. As most patients present with metastatic stage of disease, we attempt to demonstrate FGFR1 amplification in lymph node metastases of amplified primary tumors. Our study aims to give a rational to include these patients in a targeted SMI therapy. Method: We assessed 75 formalin-fixed paraffin-embedded (FFPE) primary L-SCC samples. 46 samples were primary tumours with corresponding FFPE lymph node metastasis. The biotin-labelled FGFR1 target probe (8p11.23 to 8p11.22) was used to determine the FGFR1 amplification status performing fluorescence in situ hybridization (FISH). Results: Of 39 assessable metastatic L-SCC, 7 samples displayed FGFR1 amplification (18 %). All of these primary tumors also harbored FGFR1 amplification in their lymph node metastasis. Non-amplified tumors never displayed FGFR1 amplification in corresponding metastases. Conclusion: We found FGFR1 amplification not only in primary L-SCC, but also in corresponding lymph node metastasis, suggesting that this genetic aberration is a clonal event in tumor genesis. Our study provides data indicating new therapeutic possibilities for patients suffering not only primary, but also metastatic FGFR1 amplified SCC lung cancer disease. KRAS mutation was a G to T transversion in 80 % of the smoker NSCLC population and a G to A transition in 98 % of the non smoker NSCLC population. Mutations were noted at codon 12 (90 %), codon 13 (8 %) and codon 61 (2 %). A KRAS mutation was a negative prognostic factor with a hazard ratio for death of 1.38 (95 % confidence interval, 1.16-1.63). A mucinous histological subtype was observed in more than 75 % of KRAS mutated tumours. Conclusion: KRAS oncogene substitution must be accurately determined in primary lung adenocarcinoma for correlation with tumour behaviour and clinico-pathological parameters. Objective: There is an urgent need for diagnosis of NSCLC at its early-stages and for improving the survival rate of patients. MicroRNAs, small non-coding RNAs, are frequently deregulated in NSCLC. This study aimed to explore plasma microRNAs for diagnostic value, and evaluated the correlation between expression profiles of plasma micro-RNAs and disease-free survival (DFS) in NSCLC patients. Method: We selected eighteen most frequently expressed microRNAs in NSCLC. Total plasma RNA including microRNAs was isolated and reverse-transcribed into cDNAs. The level of microRNAs was determined by quantitative real-time RT-PCR in 42 resectable NSCLC patients and 10 matched cancer-free individuals. The correlation between the expression of microRNAs in plasma and patient DFS were examined by log-rank and Cox analysis. Results: Expression levels of miR-320,−296,−145,−199a, −191,−223,−24,−152,−126, and let-7f in the plasma of NSCLC including stage-I patients were significantly higher compared with controls (P<0.0001). The combination of these microRNAs yielded 87 % sensitivity and 90 % specificity (AUC=0.934) in discriminating NSCLC patients from controls. The levels of miR-155, −152, −20a, −223, −126 and miR-199a were significantly associated with DFS (P<0.05). Conclusion: Our results suggest that high expression of 6plasma miRNAs signature would provide potential noninvasive blood-based biomarker for the prognosis of NSCLC.