Analysis of ameloblastomas by comparative genomic hybridization and fluorescence in situ hybridization
| Autor: | Toshiyuki Shibata, Róza Ádány, Makoto Toida, Tomomi Yamashita, Zsuzsa Rákosy, Keizo Kato, Margit Balázs, Andrea Treszl, Sojiro Mori, Tatsuhiko Suwa, Toshiaki Matsui, Daijiro Hatakeyama, Yutaka Yamazaki, Hiroki Makita |
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| Rok vydání: | 2005 |
| Předmět: |
Adult
Male Cancer Research Adolescent Chromosomes Human Pair 22 Gene Dosage Biology medicine.disease_cause Ameloblastoma Lesion Genetics medicine Humans Elméleti orvostudományok Molecular Biology In Situ Hybridization Fluorescence Aged Chromosome Aberrations medicine.diagnostic_test Chromosomes Human Pair 10 Nucleic Acid Hybridization Chromosome Orvostudományok Middle Aged medicine.disease Molecular biology Chromosomes Human Pair 1 Female Interphase medicine.symptom Carcinogenesis Chromosome 22 Comparative genomic hybridization Fluorescence in situ hybridization |
| Zdroj: | Cancer Genetics and Cytogenetics. 159:99-104 |
| ISSN: | 0165-4608 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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