Molecular genetic abnormalities in the pathogenesis of human lung cancer.
In the past few years our knowledge of the molecular pathogenesis of lung cancer has significantly increased. There are several molecular mechanisms involved in the multistage carcinogenesis through which respiratory epithelial cells become preneoplastic and then invasive cancer. In this review we summarize some of these changes including, genomic alterations such as loss of heterozygosity and microsatellite alterations, autocrine-paracrine loops, alterations in oncogenes and tumor suppressor genes, tumor angiogenesis, aberrant promoter methylation and inherited predisposition to lung cancer. Translation of these findings to the clinic is also discussed.
Forgacs
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University of Texas Southwestern Medical Center at Dallas, Hamon Center for Therapeutic Oncology Research, 6000 Harry Hines Blvd, Dallas 75390-8593, USA.
Zöchbauer-Müller
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S
Oláh
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Minna
J D
JD
D017209:Apoptosis; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics* / Q000378:metabolism; D018288:Carcinoma, Small Cell / Q000235:genetics* / Q000378:metabolism; D002869:Chromosome Aberrations / Q000235:genetics; D004198:Disease Susceptibility; D016147:Genes, Tumor Suppressor / Q000235:genetics*; D006133:Growth Substances / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000378:metabolism; D008745:Methylation; D008967:Molecular Biology; D009363:Neoplasm Proteins / Q000378:metabolism; D009857:Oncogenes / Q000235:genetics*; D011401:Promoter Regions, Genetic; D013234:Stem Cells; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
D006133:Growth Substances; D009363:Neoplasm Proteins; D014028:Tobacco Smoke Pollution