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| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | El-Zein, R. | en |
| dc.contributor.author | Bondy, M. L. | en |
| dc.contributor.author | Wang, L. E. | en |
| dc.contributor.author | de Andrade, M. | en |
| dc.contributor.author | Sigurdson, A. J. | en |
| dc.contributor.author | Bruner, J. M. | en |
| dc.contributor.author | Kyritsis, A. P. | en |
| dc.contributor.author | Levin, V. A. | en |
| dc.contributor.author | Wei, Q. | en |
| dc.date.accessioned | 2015-11-24T19:10:52Z | - |
| dc.date.available | 2015-11-24T19:10:52Z | - |
| dc.identifier.issn | 0143-3334 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/20878 | - |
| dc.rights | Default Licence | - |
| dc.subject | Aneuploidy | en |
| dc.subject | *Chromosome Aberrations | en |
| dc.subject | Chromosome Breakage | en |
| dc.subject | Chromosomes, Human, Pair 1/genetics | en |
| dc.subject | Female | en |
| dc.subject | Glioma/blood/*genetics | en |
| dc.subject | Humans | en |
| dc.subject | In Situ Hybridization, Fluorescence | en |
| dc.subject | Lymphocytes/cytology/*metabolism | en |
| dc.subject | Male | en |
| dc.subject | Middle Aged | en |
| dc.subject | Risk Factors | en |
| dc.title | Increased chromosomal instability in peripheral lymphocytes and risk of human gliomas | en |
| heal.type | journalArticle | - |
| heal.type.en | Journal article | en |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/10334198 | - |
| heal.identifier.secondary | http://carcin.oxfordjournals.org/content/20/5/811.full.pdf | - |
| heal.language | en | - |
| heal.access | campus | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.publicationDate | 1999 | - |
| heal.abstract | Brain tumors exhibit considerable chromosome instability (CIN), suggesting that genetic susceptibility may contribute to brain tumorigenesis. To test this hypothesis, in this pilot study, we examined for CIN in short-term lymphocyte cultures from 25 adult glioma patients and 28 age-, sex- and ethnicity-matched healthy controls (all Caucasian). We evaluated CIN by a multicolor fluorescence in situ hybridization assay using two probes: a classic satellite probe for a large heterochromatin breakage-prone region of chromosome 1 and an alpha satellite probe for a smaller region adjacent to the heterochromatin probe. Our results showed a significant increase in the mean number of spontaneous breaks per 1000 cells in glioma patients (mean +/- SD, 2.4+/-0.8) compared with controls (1.4+/-0.9; P < 0.001). By using the median number of breaks per 1000 cells in the controls as the cutoff value, we observed a crude odds ratio (OR) of 8.5 [95% confidence interval (CI) = 2.05-34.9, P < 0.001] for spontaneous breaks and brain tumor risk. After adjustment for age, sex and smoking status, the adjusted OR was 15.3 (95% CI, 2.71-87.8). A significant increase in cells with chromosome 1 aneuploidy (in the form of hyperdiploidy) (P < 0.001) was also observed in the glioma cases, with an adjusted OR of 6.6 (95% CI = 1.5-30, P < 0.05). These findings suggest that CIN can be detected in the peripheral blood lymphocytes of brain tumor patients and may be a marker for identifying individuals at risk. | en |
| heal.journalName | Carcinogenesis | en |
| heal.journalType | peer-reviewed | - |
| heal.fullTextAvailability | TRUE | - |
| Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ | |
Files in This Item:
| File | Description | Size | Format | |
|---|---|---|---|---|
| El-Zein-1999-Increased chromosoma.pdf | 99.64 kB | Adobe PDF | View/Open Request a copy |
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