Patients who fail to respond to these measures may have the dose of the EGFR inhibitor interrupted or dose

reduced. Gastrointestinal side effects including diarrhea (54%), nausea (33%), vomiting (23%), stomatitis (17%), and abdominal pain (11%) have been reported. EGFR is frequently overexpressed in gastrointestinal normal mucosa. There is evidence that EGFR is a negative regulator of chloride secretion. EGFR inhibitors could, therefore, increase chloride secretion by blocking this regulation loop and thereby inducing secretory diarrhea. Diarrhea induced by inhibitors that target the EGFR pathway can be managed easily by reducing the dose of the oral compound, which rapidly lowers the incidence and severity of diarrhea. Rarely does treatment have to be interrupted. Loperamide is a useful treatment that can decrease intestinal motility signaling pathway [49]. Like ocular complication such as conjunctivitis, hepatic as increase in Liver Function Tests, renal, hematologic

side effects including leukopenia (25%) and anemia (16%) have been reported in patients receiving cetuximab. Remarkable developments in the systemic treatment of advanced non-small-cell lung cancer have taken place over the past few years. Targeted therapies have been largely employed in patients with far advanced disease, and some of them have demonstrated consistent activity in this setting. Epidermal growth factor receptor inhibitors cause dramatic response in patients especially

with EGFR mutation. As oncology trends towards personalized therapy to reach the optimal efficacy of drug with BAY 73-4506 cost less side effect, anti EGFR and or third line TKIs have proven to be promising effective drugs in Sitaxentan lung cancer treatment as first, second and maintenance therapy which encouraging further trials in this field. Combined irreversible inhibition of EGFR revealed striking benefit compared to chemotherapy alone. The development of resistance, tumor heterogeneity, and the need to rebiopsy the tumor are all challenges that requires further study to optimize the management of patients with NSCLC. Funding: No funding sources. Competing interests: None declared. Ethical approval: Not required. “
“We have recently witnessed a remarkable progress in our understanding of molecular biology and signalling pathways of NSCLC cells which resulted in ErbB targeted therapies, ALK inhibitors and other targeted agents being now in clinical trials. However, a substantial number of NSCLC patients remain non-responsive or relapse early on these targeted therapies. Improved understanding of the functioning of ErbB receptor family have led to second generation active anti-ErbB therapies. It is clear from different preclinical and clinical studies that combined anti-ErbB therapies have a superior efficacy to single agent therapies. In future it will be essential to characterize mutations of resistance in each line of treatment.