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Erlotinib (Tarceva) is an orally bioavailable EGFR tyrosine kinase inhibitor that blocks signal transduction pathways implicated in cell proliferation and survival (1,2). Erlotinib is at the moment approved for the treatment of chemorefractory non-small cell lung cancer (NSCLC), at the same time as maintenance therapy soon after frontline chemotherapy (3,4). It truly is most active in NSCLC tumors that carry activating EGFR mutations, with only modest antitumorRequests for reprints: Bilal Piperdi, Division of Oncology, Mazer 616, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461. bpiperdi@montefiore.2628280-48-6 web org.1260385-00-9 web Zou et al.PMID:23626759 Pageactivity in NSCLC tumors that have wild form EGFR (5,six). The motives for the innate resistance to erlotinib in wild-type EGFR NSCLC tumors have not been investigated in depth. While a lot of of those tumors have an activated EGFR pathway, either such activation isn’t crucial for cell survival and proliferation or its inhibition rapidly triggers effective mechanisms of cell adaptation (7). Autophagy is usually a course of action that allows cells to sequester cytoplasmic contents by means of the formation of double-membrane vesicles (autophagosomes) and target them for degradation via their fusion with lysosomes, creating single-membrane autolysosomes (8). Emerging evidence indicates that autophagy is a self-protective cellular mechanism that provides power via the degradation and recycling of cytoplasmic contents, and promotes cell survival in response to several different stimuli (9). In add.