Abstract
In 1979, the first chromosome alteration associated with familial cancer was reported. Five years later, a fragile site was observed in the same chromosome region. The product of the fragile histidine triad (FHIT) gene, which encompasses this fragile site, is partially or entirely lost in most human cancers, indicating that it has a tumour-suppressor function. Inactivation of only one FHIT allele compromises this suppressor function, indicating that a 'one-hit' mechanism of tumorigenesis is operative. Are genes disrupted at other fragile sites? And, are these genes also tumour suppressors?
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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Adult
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Alleles
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Amino Acid Motifs
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Animals
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Apoptosis / genetics
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Cell Transformation, Neoplastic / genetics*
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Chromosome Breakage
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Chromosome Fragile Sites
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Chromosome Fragility* / genetics
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Chromosomes, Human, Pair 3 / genetics*
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Chromosomes, Human, Pair 3 / ultrastructure
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Chromosomes, Human, Pair 8 / genetics
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Chromosomes, Human, Pair 8 / ultrastructure
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Conserved Sequence
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DNA Replication
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Esophageal Neoplasms / genetics
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Esophageal Neoplasms / prevention & control
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Forecasting
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Gastrointestinal Neoplasms / chemically induced
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Gastrointestinal Neoplasms / genetics
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Gene Deletion
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Genes, Tumor Suppressor*
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Genetic Predisposition to Disease
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Genetic Therapy
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Humans
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Kidney Neoplasms / genetics
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Mice
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Mice, Knockout
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Models, Genetic
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Neoplasm Proteins / chemistry
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Neoplasm Proteins / genetics
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Neoplasm Proteins / physiology*
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Recombination, Genetic
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Structure-Activity Relationship
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Translocation, Genetic
Substances
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Neoplasm Proteins
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fragile histidine triad protein
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Acid Anhydride Hydrolases