Molecular genetic considerations in osteosarcoma.
Osteosarcoma tumorigenesis is consistent with a model by which tumorigenesis results if both alleles at the retinoblastoma susceptibility locus (RBI) are altered. Additional genetic evidence strongly suggests that another obligate event in osteosarcoma tumorigenesis is the homozygous alteration of another gene, p53. Both the RB1 gene and p53 have been proposed to act as tumor-suppressor genes, suggesting that, in this instance, tumorigenesis is the result of the loss of gene function of these two genes, rather than a gain of function.
Department of Molecular Genetics, University of Texas M.D. Anderson Cancer Center, Houston 77030.
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Hansen
D001483:Base Sequence; D015139:Blotting, Southern; D001859:Bone Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000235:genetics*; D015984:Causality; D002872:Chromosome Deletion; D002874:Chromosome Mapping; D005784:Gene Amplification; D016161:Genes, Retinoblastoma / Q000235:genetics; D016147:Genes, Tumor Suppressor / Q000235:genetics; D016158:Genes, p53 / Q000235:genetics; D014644:Genetic Variation; D006801:Humans; D008957:Models, Genetic; D008969:Molecular Sequence Data; D016296:Mutagenesis; D012516:Osteosarcoma / Q000453:epidemiology / Q000209:etiology / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D012175:Retinoblastoma / Q000150:complications / Q000235:genetics*; D014158:Transcription, Genetic