Chromosome imbalances in familial gliomas detected by comparative genomic hybridization
✍ Scribed by Niina Paunu; Satu-Leena Sallinen; Ritva Karhu; Helena Miettinen; Pauli Sallinen; Juha Kononen; Pekka Laippala; Kalle O.J. Simola; Pauli Helén; Hannu Haapasalo
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 333 KB
- Volume
- 29
- Category
- Article
- ISSN
- 1045-2257
No coin nor oath required. For personal study only.
✦ Synopsis
Familial occurrence of gliomas, in the absence of well-defined hereditary multisystem disorders, is reported occasionally. We describe 17 families that have been afflicted with two or more gliomas but do not raise suspicion of other inheritable syndromes. The families were identified among 369 consecutive glioma patients operated at the Tampere University Hospital during 1983-1994. We applied comparative genomic hybridization (CGH) analysis on 21 gliomas occurring in these 17 families. The most frequent genetic alterations, detected in over 20% of the tumors, were losses of 6q, 10, 4q, 9p and gains of 7, 19, 20q, 1p. We compared the chromosomal alterations detected in the familial gliomas to those reported previously on 209 sporadic gliomas in nine different CGH studies. In this comparison, the familial gliomas more often showed losses of chromosome arms 4q and 6q and gains of 1p and 22q. The most frequent losses (9/21 tumors) in the familial gliomas resided on chromosome arm 6q (P ϭ 0.005, Fisher's exact test; with Bonferroni correction, P ϭ 0.04). The loss of 6q was also the most common intrafamilial aberration, present in four separate gliomas belonging to two families. The minimal common area of loss on this chromosome resided at 6q14 -16. In conclusion, we have found several characteristic aberrations by CGH in the familial gliomas and we present new chromosomal regions possibly involved in the familial predisposition to gliomas.
📜 SIMILAR VOLUMES
In our case, the absence of phenotypic abnormalities indicates that the supernumerary genes present in this de novo marker do not include those which are responsible for the high pathogenicity of chromosome 16 trisomy. It would be of interest to identify the loci present in this marker. This might h
At least 50 per cent of all first-trimester spontaneous abortions are cytogenetically abnormal, including trisomy, monosomy X, triploidy, tetraploidy and structural chromosome anomalies. Traditionally, the detection of aneuploidy in fetal tissues is performed by tissue sampling, cell culturing, meta
We used comparative genomic hybridization (CGH) to evaluate DNA sequence copy number changes in 67 synovial sarcomas of both monophasic and biphasic histological subtypes. Changes (mean among aberrant cases: 4.7 aberrations/tumor; range: 1-17), affecting most often entire chromosomes or chromosome a