Abstracts Open Access
Copyright ©The Author(s) 2000. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 2000; 6(Suppl3): 78-78
Published online Sep 15, 2000. doi: 10.3748/wjg.v6.iSuppl3.78
Molecular characteristics of two esophageal carcinosarcomas: A hint for the clonality of carcinomatic and sarcomatic tumor components
MH Sun, MV Knebel Doeberitz, J Gebert, Division of Molecular Diagnostics, Department of Pathology, Institute of Pathology and Forensic Medicine, University of Heidelberg, D-69120 Heidelberg, Germany
G Mechtersheimer, Division of Therapy, Department of Pathology, Institute of Pathology and Forensic Medicine, University of Heidelberg, D-69120 Heidelberg, Germany
P Moeller, Department of Pathology, University of Ulm, Albert Einstein Allee 11, D-89081 Ulm, Germany
MH Sun, Laboratory of Molecular Pathology, Department of Pathology, Cancer Hospital/Cancer Institute, Shanghai Medical University 200032 Shanghai, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. J Gebert, Division of Molecular Diagnostics and Therapy, University of Heidelberg, D-69120 Heidelberg, Germany. Johannes Gebert@med.uni-heidelberg
Telephone: 6221-566165(lab)
Received: April 24, 2000
Revised: June 10, 2000
Accepted: July 10, 2000
Published online: September 15, 2000

Abstract

AIM: To study the clonality of the esophageal carcinosarcoma by using molecular approaches.

METHODS: Two esophageal carcinosarcomas were included in the study. Tumor area from dysplastic lesion, squamous cell carcinoma, basaloid cell carcinoma and spindle cell elements were microdissected separately. Each element was analyzed with 14 microsatellite markers and direct sequenced for p53 gene and ras gene mutation.

RESULTS: Both tumors displayed a typical histologic feature of carcinosarcoma. Both cases showed the divergent differentiation by immunohistochemistry study. In case 1 the identical LOH at p53 and hMLH1 loci was detected. The heterogenous LOH was detected only in carcinosarcoma at RB1 and BRCA1 loci, while the LOH at ACTC locus was seen only in sarcoma. The same mutation of the splice site of exon 6-intron 6 displayed in the two tumor elements. In case 2, a coordinate LOH at RB locus was demonstrated in three types of tumor elements: squamous carcinoma, basaloid carcinoma and spindle cell element. A heterogenous LOH was seen only in spindle cells at TAP1 locus. No mutation in exon 5-8 of p53 gene has been found in case 2. No mutation of K-ras gene was found.

CONCLUSION: Although the different differentiation, the two elements of esophageal carcinosarcoma may have a single clonality. The p53 gene mutation occurred before the two differentiation directions switched. The distinct molecular genotype can be determined through molecular biological analysis. The microsatellite profiling can serve as an approach to find out which genetic alteration occurs before or after the differentiation is determines.

Key Words: Esophageal neoplasms; Mutation; Genes, p53; Molecular biology; Heterozygosity loss

Footnotes

E- Editor: Zhang FF

$[References]