In this study, we analyzed 10 human squamous cell carcinomas (SCCs) for alterations in the p53 tumor suppressor gene in exons 4 through 9 by single-strand conformation polymorphism (SSCP) analysis. We found that 2 of 10 SCCs displayed unusual SSCP alleles at exon 7 of the p53 gene. Subsequent clonin
Aberrations of tumor-suppressor genes (p53, apc, mcc and Rb) in esophageal squamous-cell carcinoma
โ Scribed by Chihaya Maesawa; Gen Tamura; Yasushi Suzuki; Satoshi Ogasawara; Kaoru Ishida; Kazuyoshi Saito; Ryoichi Satodate
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- French
- Weight
- 751 KB
- Volume
- 57
- Category
- Article
- ISSN
- 0020-7136
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โฆ Synopsis
Loss of heterozygosity at 4 tumor-suppressor gene loci (pS3, apc, mcc and Rb) was investigated using polymerase chain reactions, in 49 esophageal squamous-cell carcinoma specimens from patients who had undergone curative resection. Mutations in the p53 gene within exons 5 to 8 were also examined. LOH was detected in 9 (43%) of 21 p53 genes, 16 (55%) of 29 apc genes, 10 (48%) of 21 rncc genes, and 13 (52%) of 25 Rb genes for which heterozygosity could be determined. Mutations in the p53 gene were detected in 18 (36%) of 49 cases and were significantly more frequent in stage-Ill tumors and in tumors exhibiting DNA aneuploidy. In 5 cases where heterozygosity could be determined for all the loci, all had 2 or more aberrations. Additionally, a heterozygous deletion of p53 gene was associated with a mutation of the remaining allele in 8 (89%) of 9 cases. Short-term relapse within 3 to 12 months occurred significantly more frequently in patients having tumors with both p53 aberrations (p < 0.05). Thus, aberration of tumor-suppressor genes was a frequent occurrence in esophageal squamous-cell carcinoma and inactivation of the p53 gene may contribute to the progression of this tumor.
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