Author/Authors :
Toida، نويسنده , , Makoto and Balلzs، نويسنده , , Margit and Treszl، نويسنده , , Andrea and Rلkosy، نويسنده , , Zsuzsa and Kato، نويسنده , , Keizo and Yamazaki، نويسنده , , Yutaka and Matsui، نويسنده , , Toshiaki and Suwa، نويسنده , , Tatsuhiko and Hatakeyama، نويسنده , , Daijiro and Makita، نويسنده , , Hiroki and Mori، نويسنده , , Sojiro and Yamashita، نويسنده , , Tomomi and Shibata، نويسنده , , Toshiyuki a، نويسنده ,
Abstract :
In order to characterize the chromosomal alterations in ameloblastomas, a combination of comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH) techniques was performed on 9 tumors. Chromosomal alterations including a gain at 1q and losses at 1pter, 10q, and 22q could be detected by CGH only in 1 tumor. Interphase FISH analysis, using centromeric probes for chromosomes 1, 10, and 22 as well as region-specific probes for 1p36 and 10q26, revealed the most frequent alterations to exist in the tumor with the abnormal CGH profile. These alterations included marked to slight increases of monosomic cells for chromosome 10 (91.5%), 10q26 (35.8%), 1p36 (24.4%), and chromosome 22 (18.8%), as well as significant elevations of trisomic cells for chromosome 1 (41.2%). Moreover, FISH analysis revealed a frequent loss of chromosome 22 in all tumors examined, except for one lesion, indicating that loss of the entire or a part of this chromosome is a common event in ameloblastomas, possibly being a predisposing factor to ameloblastoma tumorigenesis.
