Genetic mechanisms in esophageal carcinogenesis: Frequent deletion of 3p and 17p in premalignant lesions

✍ Scribed by Mamoru Shimada; Akio Yanagisawa; Yo Kato; Masatoshi Inoue; Hitoshi Shiozaki; Morito Monden; Yusuke Nakamura

• Book ID: 101259936
• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 462 KB
• Volume: 15
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/(sici)1098-2264(199603)15:3<165::aid-gcc3>3.0.co;2-0

✦ Synopsis

Atthough dysplasia of the esophagus is thought to be the precursor lesion of esophageal squamow 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 I06 lesions among 32 patients with ESC. Allelic losses on 3p or I7p occurred frequently even in dysplastic lesions (9 o f 21 and I 3 of 24 samples, respectively) including lesions with mild dysplasia (3p, 4 of I0 samples; I7p, 6 of I 4 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 I7p 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.