Abstract
The status of the p53 gene of tumor cells can modify the sensitivity of the tumors to radiation and anti-cancer agents. Human esophageal cancer cells (T.Tn) bearing mutated p53 gene were retrovirally transduced with wild-type p53 gene. The transduced cells (T.Tn/p53) which stably expressed wild-type p53 proliferated at the same rate as parental cells. However, the sensitivity to radiation was significantly improved by the transduction and T.Tn/p53 cells became markedly susceptible to cisplatin and etoposide compared with parental cells. Administration of cisplatin noticeably suppressed the growth of T.Tn/p53 tumors but not T.Tn tumors inoculated in nude mice. Forced expression of wild-type p53 gene thereby can increase the sensitivity to DNA damage in esophageal cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology*
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Antineoplastic Agents, Phytogenic / pharmacology
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Carcinoma / drug therapy
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Carcinoma / genetics*
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Carcinoma / radiotherapy
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Cell Division / drug effects
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Cisplatin / pharmacology
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Esophageal Neoplasms / drug therapy
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Esophageal Neoplasms / genetics*
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Esophageal Neoplasms / radiotherapy
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Etoposide / pharmacology
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Female
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Gene Expression Regulation, Neoplastic
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Genes, p53*
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Humans
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Mice
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Mice, Inbred BALB C
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Mice, Nude
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Microbial Sensitivity Tests
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Mutation
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Neoplasm Transplantation
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Radiation Tolerance*
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Retroviridae / genetics
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Transduction, Genetic
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Tumor Suppressor Protein p53 / biosynthesis
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / physiology*
Substances
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Antineoplastic Agents
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Antineoplastic Agents, Phytogenic
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Tumor Suppressor Protein p53
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Etoposide
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Cisplatin