Abstract
A new era in the treatment of malignant diseases has been observed through the use of biologic agents targeting growth factor receptors, signaling pathways, gene mutations and others. The results have been impressive in some diseases and modest in others. The discovery of new targets has expanded our knowledge of different mechanisms in tumorigenesis. One of these mechanisms has been DNA methylation, which is an important gene transcription regulator. Although the role of methylation in lung carcinogenesis is not well understood, there is an enormous quantity of evolving data suggesting its critical role in lung cancer. In this review, the authors will discuss methylation in lung carcinogenesis and its possible clinical implications.
MeSH terms
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Apoptosis Regulatory Proteins
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Calcium-Calmodulin-Dependent Protein Kinases / genetics
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism
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Cell Transformation, Neoplastic*
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Clinical Trials as Topic
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Cyclin-Dependent Kinase Inhibitor p16 / genetics
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Cyclin-Dependent Kinase Inhibitor p16 / metabolism
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DNA Methylation*
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Death-Associated Protein Kinases
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Humans
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Lung Neoplasms / drug therapy
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Lung Neoplasms / genetics*
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Lung Neoplasms / physiopathology*
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Mutation
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Promoter Regions, Genetic
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Signal Transduction
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Transcription, Genetic
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism
Substances
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Apoptosis Regulatory Proteins
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Cyclin-Dependent Kinase Inhibitor p16
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RASSF1 protein, human
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Tumor Suppressor Proteins
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Death-Associated Protein Kinases
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Calcium-Calmodulin-Dependent Protein Kinases