Cyclin D1 gene amplification in esophageal carcinosarcoma shown by differential polymerase chain reaction

• Published in: Human pathology Vol. 29; no. 7; pp. 662 - 667
• Main Authors: Suzuki, Hiroaki, Moriya, Jun, Nakahata, Atsuko, Fujioka, Yasunori, Inoue, Kazuaki, Nagashima, Kazuo
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.07.1998; Elsevier
• Subjects: Biological and medical sciences; Blotting, Southern; carcinosarcoma; Carcinosarcoma - genetics; Carcinosarcoma - metabolism; Carcinosarcoma - pathology; cyclin D1; Cyclin D1 - genetics; differential PCR assay; DNA Primers - chemistry; DNA, Neoplasm - analysis; Esophageal Neoplasms - genetics; Esophageal Neoplasms - metabolism; Esophageal Neoplasms - pathology; Esophagus; Gastroenterology. Liver. Pancreas. Abdomen; Gene Amplification; HeLa Cells; Humans; Immunoenzyme Techniques; Medical sciences; p53; Polymerase Chain Reaction; Receptors, Dopamine D2 - genetics; Tumor Suppressor Protein p53 - metabolism; Tumors; carcinosarcoma; CD; cyclin D1; DPCR; cdk; esophagus; differential PCR assay; DR; p53; Human; Immunohistochemistry; Esophageal disease; Cyclin; Malignant tumor; Gene expression; Cyclin D1; Carcinogenesis; Esophagus; Case study; Polymerase chain reaction; Pathology; TP53 Gene; C-Onc gene; Digestive diseases; Molecular biology; Differentiation; Southern blotting; Protooncogene; Spindle cell carcinoma; Tumor suppressor gene
• ISSN: 0046-8177; 1532-8392
• DOI: 10.1016/S0046-8177(98)90273-8

We studied cyclin D1 gene amplification in four esophageal carcinosarcomas using the differential polymerase chain reaction. Three cases showed amplification in the sarcomatous components, and one of these also showed amplification in the carcinomatous component. No amplification was detected in the other case. We also examined p53 expression in these four tumors by immunostaining. Both components of all four cases showed diffuse overexpression of p53 protein in the nuclei. Our results showed that the cyclin D1 gene is frequently amplified in esophageal carcinosarcoma, especially in the sarcomatous component. Two cases showed amplification only in the sarcomatous component, suggesting that amplification may have a role in the pathogenesis of that component of this malignancy. The diffuse overexpression of p53 observed in both components suggests that such overexpression, which could be the result of somatic mutation, might be an early event in the pathogenesis of esophageal carcinosarcoma.