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KMID : 0982820040030010001
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Journal of Lung Cancer
2004 Volume.3 No. 1 p.1 ~ p.5
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Incidence and Risk Factors of Postpneumonectomy Pulmonary Edema with Non-Small Cell Lung Cancer: A Retrospective AnalysisThe Role of Phosphatase and Tensin Homolog Deleted on Chromosome Ten (PTEN) in Lung Cancer
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Lee Ho-Kyung
Lee Yong-Chul
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Abstract
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Lung cancer remains the primary cause of cancer-related death in the world, and the number of cases continues to increase. Like any other human cancer, the development of lung cancer is associated with the activation of oncogenes or inactivation of tumor suppressor genes. Phosphatase and tensin homolog, deleted on chromosome ten (PTEN), is a part of a complex signaling system that affects a variety of important cell functions. PTEN opposes the action of phosphatidylinositol 3-kinase (PI3-kinase) by dephosphorylating the signaling lipid phosphatidylinositol 3, 4, 5-triphosphate (PIP3). In addition, it displays weak tyrosine phosphatase activity, which may down modulate the signaling pathways involving focal adhesion kinase (FAK) or Shc. Functions for PTEN have been identified in the regulation of many normal cell processes, including growth, adhesion, migration, invasion and apoptosis. PTEN appears to play particularly important roles in regulating anoikis (apoptosis of cells after loss of contact with extracellular matrix) and cell migration. Many studies have suggested that the loss of PTEN expression occurs commonly in primary lung cancers and correlates with the histological type. Regulation of PTEN expression may provide a new preventive and therapeutic modality in primary lung cancer. However, there is, in our opinion, a need for further study of this gene.
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KEYWORD
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Lung cancer, Phosphatidylinositol 3-kinase, Signal transduction.Abbreviations: PTEN, phosphatase and tensin homolog deleted on chromosome ten, PI3-kinase, phosphatidylinositol 3-kinase, PIP3, phosphatidylinositol 3, 4, 5-triphosphate, FAK, focal adhesion
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