Abstract
Gene amplification in stomach and oesophageal cancers was reviewed. In stomach cancers, two receptor type tyrosine kinases, c-erbB-2 and K-sam, are frequently amplified and overexpressed. c-erbB-2 seems to be preferentially amplified in well-differentiated, and K-sam in poorly-differentiated, gastric adenocarcinomas. 11q13 genes are amplified in about 50% of the oesophageal cancers. These genes include hst-1, int-2 and cyclin D/prad1, all of which are mapped to chromosome 11 at band q13. Although hst-1 and int-2 are usually not expressed despite amplification, elevated transcription of the cyclin D gene is accompanied by its amplification, suggesting a role of a G1 cyclin in oesophageal carcinogenesis.
MeSH terms
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ErbB Receptors / genetics
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Esophageal Neoplasms / genetics*
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Fibroblast Growth Factor 3
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Fibroblast Growth Factor 4
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Fibroblast Growth Factors / genetics
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Gene Amplification*
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Humans
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Neoplasm Proteins / genetics*
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Oncogenes*
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Proto-Oncogene Proteins / genetics
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Receptor Protein-Tyrosine Kinases*
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Receptor, ErbB-2
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Receptor, Fibroblast Growth Factor, Type 2
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Receptors, Fibroblast Growth Factor*
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Stomach Neoplasms / genetics*
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Transcription, Genetic
Substances
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FGF3 protein, human
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FGF4 protein, human
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Fibroblast Growth Factor 3
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Fibroblast Growth Factor 4
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Neoplasm Proteins
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Proto-Oncogene Proteins
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Receptors, Fibroblast Growth Factor
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Fibroblast Growth Factors
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ErbB Receptors
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FGFR2 protein, human
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Receptor Protein-Tyrosine Kinases
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Receptor, ErbB-2
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Receptor, Fibroblast Growth Factor, Type 2