Loss of heterozygosity on chromosomes 3 and 11 in a radiation-induced malignant fibrous histiocytoma - Case report
Journal
Journal of the Otolaryngological Society of the Republic of China
Journal Volume
33
Journal Issue
1
Pages
86-91
Date Issued
1998
Author(s)
Abstract
Malignant transformation in tumor development results from a series of genetic changes and the inactivation of tumor suppressor genes is among the most common molecular events that contribute to tumorigenesis. Although a variety of mechanisms exsist for the inactivation of tumor suppressor genes, loss of chromosomal segments in tumor cells has proven common and useful in mapping regions containing putative tumor suppressor genes. Loss of one homologous chromosomal segment means loss of heterozygosity (LOH) (hemizygous deletion). Microsatellite polymorphic markers consist of CA dinucleotide repeats and often display extensive length polymorphism. LOH on the chromosomes 3, 9, 11 by means of microsatellite markers has been found in squamous cell carcinomas of the head and neck. The radiation-induced malignant fibrous histiocytoma in the head and neck region is rare and grows very rapidly with a poor prognosis. To detect LOH in this cancer, we analysed microsatellite polymorphism in the tumor tissue and peripheral lymphocytes of a patient with radiation-induced malignant fibrous histiocytoma. Fifty-three microsatellite polymorphic markers with corresponding pairs of primers labelled with fluorescent on chromosomes 3, 9 and 11 were used. The respective DNA's of the cancer cells and normal lymphocytes were amplified with polymerase chain reaction (PCR). We analysed the PCR products on a Model 377 DNA Analysis System (Perkin-Elmer/Applied Biosystems Division) using the GeneScan(TM) software. LOH was found on one marker of chromosome arm 3p (D3S1300), two markers of chromosome arm 3q (D3S1262, D3S1311), and one marker of chromosome arm 11p (DllS922).
SDGs
Other Subjects
adult; article; carcinogenesis; case report; chromosome 11; chromosome 3; chromosome 9; dermatofibroma; dermatofibrosarcoma protuberans; gene deletion; genetic susceptibility; heterozygosity loss; human; male; malignant transformation; polymerase chain reaction; tumor suppressor gene
Type
journal article