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Aberrations of tumor‐suppressor genes ( p53 , apc , mcc and Rb ) in esophageal squamous‐cell carcinoma
Author(s) -
Maesawa Chihaya,
Tamura Gen,
Suzuki Yasushi,
Ogasawara Satoshi,
Ishida Kaoru,
Saito Kazuyoshi,
Satodate Ryoichi
Publication year - 1994
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910570105
Subject(s) - loss of heterozygosity , tumor suppressor gene , biology , cancer research , gene , exon , epidermoid carcinoma , mutation , carcinoma , allele , microbiology and biotechnology , carcinogenesis , genetics
Loss of heterozygosity at 4 tumor‐suppressor gene loci ( p53 , 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 mcc 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‐III 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. © Wiley‐Liss, Inc.