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Genetic mechanisms in esophageal carcinogenesis: Frequent deletion of 3p and 17p in premalignant lesions
Author(s) -
Shimada Mamoru,
Yanagisawa Akio,
Kato Yo,
Inoue Masatoshi,
Shiozaki Hitoshi,
Monden Morito,
Nakamura Yusuke
Publication year - 1996
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199603)15:3<165::aid-gcc3>3.0.co;2-0
Subject(s) - dysplasia , carcinogenesis , esophagus , pathology , biology , allele , esophageal cancer , carcinoma , loss of heterozygosity , tumor suppressor gene , intraepithelial neoplasia , lesion , esophageal disease , epidermoid carcinoma , cancer research , cancer , gene , genetics , medicine , prostate , anatomy
Although dysplasia of the esophagus is thought to be the precursor lesion of esophageal squamous cell carcinoma (ESC), the sequence of genetic events during esophageal carcinogenesis is unclear. Using the polymerase chain reaction, we examined allelic losses at microsatellite loci in DNAs isolated from 106 lesions among 32 patients with ESC. Allelic losses on 3p or 17p occurred frequently even in dysplastic lesions (9 of 21 and 13 of 24 samples, respectively) including lesions with mild dysplasia (3p, 4 of 10 samples; 17p, 6 of 14 samples, respectively), and allelic losses on these chromosomal arms were also observed in cancerous tissues. We also detected allelic losses of the short and long arms of chromosome 9 at a low frequency in lesions with mild dysplasia and often in lesions with severe dysplasia and in intraepithelial cancers. Our results suggested that inactivation of tumor suppressor genes on 3p and 17p occurs at a very early stage of esophageal carcinogenesis and that genes on 9p and 9q are likely to play important roles in malignant changes. Comparison of the genetic alterations in precancerous dysplastic lesions with those in carcinomas supports the idea that ESC arises from the dysplastic lesion. Genes Chromosom Cancer 15:165–169 (1996). © 1996 Wiley‐Liss, Inc.

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