Gene amplification and TP53 mutations in an experimental model of colorectal cancer
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文摘
Tumor cells and cultured cell lines spontaneously generate drug-resistant variants that contain amplified DNA when cells are exposed to selective agents that block DNA or RNA synthesis. By contrast, normal diploid cells do not show any evidence of gene amplification in the same conditions. Recent data suggested that one of the control mechanisms of normal cells can be mediated by the TP53 gene. Using fibroblasts from patients with the Li-Fraumeni syndrome, it was shown that the ability to amplify correlates with the presence of a mutated TP53 gene and the loss of the wild type allele.

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