Abstract
The development and progression of lung cancer is a multistep process characterized by the accumulation of numerous genetic and epigenetic alterations, some of which occur early in the course of disease. In this review, we summarize cytogenetic imbalances and molecular genetic/epigenetic changes seen in human small-cell and non-small-cell lung cancer. Alterations of tumor suppressor genes and oncogenes leading to perturbations of key cell-regulatory and growth-control pathways are highlighted. The translational implications of molecular biomarkers for risk assessment, early detection, and monitoring of chemoprevention trials are discussed.
Copyright 2002 Wiley-Liss, Inc.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Acid Anhydride Hydrolases*
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Chromosomes, Human, Pair 3
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Cytogenetics*
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Gene Silencing
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Genes, p16
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Humans
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Lung Neoplasms / genetics*
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Neoplasm Proteins / genetics
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Proto-Oncogene Proteins c-myc / genetics
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Proto-Oncogene Proteins c-myc / metabolism
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Retinoblastoma Protein / genetics
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Sequence Deletion
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
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ras Proteins / genetics
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ras Proteins / metabolism
Substances
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Neoplasm Proteins
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Proto-Oncogene Proteins c-myc
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Retinoblastoma Protein
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Tumor Suppressor Protein p53
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fragile histidine triad protein
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Acid Anhydride Hydrolases
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ras Proteins