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Lung cancer remains a serious public health problem and is the first cause of cancer death worldwide, and the overall 5-year survival rate for all stages is 14-17 % for Non-small-cell lung cancer and 6 % for small-cell lung cancer. Clinical and epidemiologic studies have suggested a strong association among chronic infection, inflammation, and cancer. Immune system plays a critical role in maintaining tissue homeostasis, cell turnover, tissue remodeling, and preventing infection and cell transformation. The inflammatory component in the development of the neoplasm includes a diverse leukocyte population; these components are considered inflammatory tumor key factors promoting tumor progression due to its ability to release a variety of cytokines, chemokines, and cytotoxic mediators such as reactive oxygen species (ROS), metalloproteinases, interleukins, and interferons. Cancer-related inflammation affects many aspects of malignancy, including the proliferation and survival of malignant cells, angiogenesis, tumor metastasis, and tumor response to chemotherapeutic drugs and hormones. Moreover, epidemiologic studies and meta-analysis have shown that prolonged use of non-steroid anti-inflammatory (NSAID) drugs reduces the risk of several solid tumor including lung cancer. Strong lines of evidence suggest that the chemopreventive properties of chronic NSAID administration are based on their COX-inhibitory activity. However, the prevention is a much better and more economical way to fight against cancer than treating an already advanced and often incurable disease.

Introduction The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion Most of the TKR share intracellular signaling pathways; therefore, cancer cells tend to overcome the inhibition of one tyrosine kinase receptor by activating another. The future of TKI (Tyrosine Kinase Inhibitor) therapy will potentially come from multi-targeted TKIs that target different TKR simultaneously. It is crucial to understand the interaction of the FGF-FGFR axis with other known driver TKRs. Based on this, it is possible to develop therapeutic strategies targeting multiple connected TKRs at once. One correct step in this direction is the reassessment of multi target inhibitors considering the FGFR status of the tumor. Another opportunity arises from assessing the use of FGFR TKI on patients harboring FGFR alterations