title: Intracellular signals of lung cancer cells as possible therapeutic targets.
abstract: In recent years, several molecularly targeted therapies have been developed as part of lung cancer treatment; they have produced dramatically good results. However, among the many oncogenes that have been identified to be involved in the development of lung cancers, a number of oncogenes are not covered by these advanced therapies. For the treatment of lung cancers, which is a group of heterogeneous diseases, persistent effort in developing individual therapies based on the respective causal genes is important. In addition, for the development of a novel therapy, identification of the lung epithelial stem cells and the origin cells of lung cancer, and understanding about candidate cancer stem cells in lung cancer tissues, their intracellular signaling pathways, and the mechanism of dysregulation of the pathways in cancer cells are extremely important. However, the development of drug resistance by cancer cells, despite the use of molecularly targeted drugs for the causal genes, thus obstructing treatment, is a well-known phenomenon. In this article, we discuss major causal genes of lung cancers and intracellular signaling pathways involving those genes, and review studies on origin and stem cells of lung cancers, as well as the possibility of developing molecularly targeted therapies based on these studies.
authors.affiliation: Department of Stem Cell Pathology, Kansai Medical University, Hirakata, Japan.
authors.forename: Kiyomichi
authors.initials: K
authors.lastname: Tanaka
authors.affiliation: Department of Stem Cell Pathology, Kansai Medical University, Hirakata, Japan.
authors.forename: Keiki
authors.initials: K
authors.lastname: Kumano
authors.affiliation: Department of Stem Cell Pathology, Kansai Medical University, Hirakata, Japan.
authors.forename: Hiroo
authors.initials: H
authors.lastname: Ueno
mesh_terms: D000818:Animals; D015820:Cadherins / Q000235:genetics / Q000378:metabolism; D019008:Drug Resistance, Neoplasm; D044127:Epigenesis, Genetic; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D035683:MicroRNAs / Q000378:metabolism; D058990:Molecular Targeted Therapy / Q000379:methods; D014411:Neoplastic Stem Cells / Q000187:drug effects / Q000378:metabolism; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D051880:Receptors, Notch / Q000235:genetics / Q000378:metabolism; D055748:SOXB1 Transcription Factors / Q000235:genetics / Q000378:metabolism; D050791:STAT Transcription Factors / Q000378:metabolism; D015398:Signal Transduction; D060449:Wnt Signaling Pathway
chemical_list: D015820:Cadherins; D035683:MicroRNAs; D051880:Receptors, Notch; C527782:SOX2 protein, human; D055748:SOXB1 Transcription Factors; D050791:STAT Transcription Factors; D011505:Protein-Tyrosine Kinases
keywords: Lung cancer; lung cancer stem cells; lung stem cells; molecularly targeted therapy; survival signals