title: Epithelial Mesenchymal Transition in Aggressive Lung Cancers.
abstract: The progression of a cancer cell into a metastatic entity contributes to more than 90 % of cancer related deaths. Therefore, the prevention and treatment of metastasis is an unmet clinical need. Epithelial to mesenchymal transition (EMT) is an evolutionary conserved developmental program, which is induced during cancer progression and contributes to metastatic colonization. EMT endows metastatic properties upon cancer cells by enhancing mobility, invasion, and resistance to apoptotic stimuli. Furthermore, EMT-derived tumor cells acquire stem cell properties and exhibit therapeutic resistance. The disseminated tumor cells recruited to distant organs are suggested to subsequently undergo an EMT reversion through mesenchymal to epithelial transition (MET), necessary for efficient colonization and macrometastasis. A major focus of cancer research is to determine the cellular and molecular mechanisms underlying EMT/MET in tumor invasion, dissemination and metastasis. In this chapter, we will focus on the contribution of the EMT signaling pathways in lung cancer progression, cancer stem cells and acquired resistance to EGFR tyrosine kinase inhibitors and chemotherapy. We will also discuss the potential of targeting EMT pathways as an attractive strategy for the treatment of lung cancer.
authors.affiliation: Department of Cardiothoracic Surgery, Neuberger Berman Foundation Lung Cancer Center, New York, NY, 10065, USA. vim2010@med.cornell.edu.|Department of Cell and Developmental Biology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY, 10065, USA. vim2010@med.cornell.edu.
authors.forename: Vivek
authors.initials: V
authors.lastname: Mittal
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects* / Q000235:genetics; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008207:Lymphatic Metastasis; D058990:Molecular Targeted Therapy; D009154:Mutation; D009361:Neoplasm Invasiveness; D014411:Neoplastic Stem Cells / Q000378:metabolism / Q000473:pathology; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D015398:Signal Transduction
chemical_list: D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D047428:Protein Kinase Inhibitors; C512478:EGFR protein, human; D066246:ErbB Receptors
keywords: Cancer stem cells; Epithelial mesenchymal transition; Lung cancer; Metastasis; Resistance; Therapy