Personalized medication therapy in patients with aN advanced lung adenocarcinoma

State of the Art is a report on the contemporary models of drug treatment of advanced NSCLC and its major representative - the adenocarcinoma. This subcategory possesses individual metabolic enzyme activity, which could be a specific target of the antitumor therapy. Its histology is a potential predictor for the result of the chemotherapy. Adenocarcinoma has an intensive immunohistochemical expression of timidilat synthetase (TS).The histologic subtypes have specific genetic profile , modifying the effect of the target therapy.The mutational status of the receptor for the epidermal growth factor (EGFR) determines the intracellular signal pathways, which regulate the proliferation, invasion, metastasis, angiogenesis and apoptosis. The rearrangement of the receptor of the tyrosine kinase of the anaplastic lymphoma (ALK) is relevant to the cellular cycle, metabolism and survival of the tumor cells. The tumor angiogenesis is defined by ligands of the growth factor of the vessel endothelium (VEGF) activating the signal pathways.The described molecular -pathologic and genetic features of NSCLC determine some of the treatment models: (1) administer agents, inhibitors of TS (antifolates)I¾ (2) necessity of testing the EGFR mutation status, as a predicting marker of the effect of the EGFR tyrosine kinase inhibitors and the changes of ALK gen, as a predicting marker of the ALK inhibitorsI¾ (3) first line target therapy in tumors with EGFR mutation(significantly prolongs progression free survival)I¾(4) second line target therapy in NSCLC, which is positive for ALK rearrangement and has progression after one line of chemotherapy ( significantly superior than the second line classic chemotherapy)I¾ (6) adding antiangiogenesic treatment as a first line therapy or as a supportive therapy.