NSCLC patients who smoked tobacco/cigarettes differed from those having a background of WSE regarding tumor histology, mutation profile, response rate, and OS, indicating that different carcinogenic mechanisms were induced by these two types of smoke exposure.

KRAS mutation status is a good biomarker for response to EGFR-TKIs in patients with NSCLC. KRAS mutational status could impact the decision to give CT or EGFR-TKIs as a second line of treatment to patients with NSCLC, particularly in patients with WT-EGFR.

Background: Subdividing non-small cell lung cancer (NSCLC) based on molecular alterations such as EGFR, KRAS and ALK genes is important for selecting treatment involving EGFR and EML4-ALK tyrosine kinase inhibitors (TKI). However, little information is available comparing patients' response and progression-free survival in the presence or absence of EGFR, KRAS mutations or the EML4-ALK fusion gene when being treated with chemotherapy. Methods: NSCLC patients were treated with chemotherapy and/or TKIs. Tests were performed for EGFR and KRAS gene mutation as well as EML4-ALK fusion genes. Progression-free survival and overall survival association with type of treatment and mutational status was analyzed. Results: The factors associated with a response to chemotherapy were the presence of EGFR and KRAS mutation (p = 0.006 and p = 0.028, respectively). Factors associated with TKI response were adenocarcinoma (HR 2.7: 1.6–4.6 95%CI; p<0.001), EGFR mutation (HR 0.5: 0.3–0.8 95%CI; p = 0.009) and wild-type KRAS (HR 1.7: 1.1–2.8 95%CI; p = 0.013). Mean progression-free survival in the chemotherapy group was 5.3 months (4.8–5.7 95%CI). Conclusion: EGFR and KRAS mutation status appeared to subdivide NSCLC patients into TKI and chemotherapy response groups.

, 748 patients with a diagnosis of advanced NSCLC and CEA levels >20 ng/mL were included in the analysis. The median age was 60.2 years old, 631 patients (84.4%) had adenocarcinoma histology. From 338 patients evaluated for EGFR mutations, 139 (31.3%) harboured an EGFR mutation. The median OS was 23.3 months (95% CI 19.4-26.9) in patients who completely normalized CEA vs 10.0 months (95% CI 8.9-11.2) in patients who did not achieve CEA normalization, with an HR 0.48 95% CI (0.35-0.67) p <0.0001. The median OS was 15.5 months (95% CI 13.4-17.6) in patients who showed a decrease in CEA levels vs 8.8 months (95% CI 7.5-10.1) in those who did not. Reduction in CEA levels was associated with better OS, either in patients treated with TKI or platinum-based chemotherapy. Conclusion: Although previous studies have suggested a possible relation between CEA levels and clinical outcome, its utility in the clinic has been controversial. In this study, we demonstrate normalization of serum CEA levels is related to longer OS rates and could be useful as an indirect biomarker for treatment response evaluation. Hence, we suggest its determination for the standard follow-up of advanced NSCLC patients under TKI or platinum-based chemotherapy treatment.