| Affiliation: | (1) Department of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan;(2) Theranostics Research Center (TRC), Otsuka Pharmaceutical Co., 463-10 Kagasuno Kawauchi-cho, Tokushima 771-0192, Japan;(3) Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), 4-1-8 Honmachi, Kawaguchi 332-0012, Japan;(4) Fujisaki Cell Center, Hayashibara Biochemical Laboratories, 675-1 Fujisaki, Okayama 702-8006, Japan;(5) Department of Hematology, University of Cambridge Clinical School, MRC Centre, Hills Road, Cambridge, CB2 2QH, United Kingdom |
| Abstract: | Comparative genomic hybridization (CGH) analyses have detected gains of copy number on 13q, especially at 13q31-q32, in cell lines and primary cases of various types of lymphoma. Since amplification of chromosomal DNA is one of the mechanisms that can activate tumor-associated genes, and because 13q amplification had been reported in various other types of tumors as well, we attempted to define by fluorescence in situ hybridization (FISH) a common region at 13q31-q32 in which to explore genes that might be targets for the amplification events. Although the commonly amplified region we defined was relatively large (approximately 4 Mb), only one true gene, GPC5, was found there. GPC5 was over-expressed in lymphoma cell lines that had shown amplification, in comparison with those that had not. Our findings suggest that GPC5 is a likely target for amplification, and that over-expression of this gene may contribute to development and/or progression of lymphomas and other tumors. |
