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?
Pubmed ID: 11902576 RIS Download
Mesh terms: Acid Anhydride Hydrolases | Adult | Alleles | Amino Acid Motifs | Animals | Apoptosis | Cell Transformation, Neoplastic | Chromosome Breakage | Chromosome Fragile Sites | Chromosome Fragility | Chromosomes, Human, Pair 3 | Chromosomes, Human, Pair 8 | Conserved Sequence | DNA Replication | Esophageal Neoplasms | Forecasting | Gastrointestinal Neoplasms | Gene Deletion | Genes, Tumor Suppressor | Genetic Predisposition to Disease | Genetic Therapy | Humans | Kidney Neoplasms | Mice | Mice, Knockout | Models, Genetic | Neoplasm Proteins | Recombination, Genetic | Structure-Activity Relationship | Translocation, Genetic
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