Trisomy 7 in synovial fluid cells of patients with rheumatoid arthritis

Tascioglu F., Durak B., Oner C., Artan S.

RHEUMATOLOGY INTERNATIONAL, cilt.25, sa.8, ss.571-575, 2005 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 25 Sayı: 8
  • Basım Tarihi: 2005
  • Doi Numarası: 10.1007/s00296-004-0477-6
  • Dergi Adı: RHEUMATOLOGY INTERNATIONAL
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.571-575
  • Anahtar Kelimeler: cytogenetics, fluorescence in situ hybridisation, rheumatoid arthritis, trisomy 7, CLONAL CHROMOSOME-ABERRATIONS, TUMOR-SUPPRESSOR GENE, SOMATIC MUTATIONS, IN-VIVO, OSTEOARTHRITIS, ASSOCIATION, TISSUE
  • Eskişehir Osmangazi Üniversitesi Adresli: Evet

Özet

Objective: Recent studies revealed trisomy 7 as a chromosomal abnormality in non-neoplastic disorders such as rheumatoid arthritis (RA). In the present study, we investigated the presence of trisomy 7 in the synovial fluid cells of patients with RA using fluorescence in situ hybridisation (FISH) analysis. Methods: Synovial fluid from 15 patients with RA was collected from knee joints. The control group consisted of seven patients with traumatic synovial effusion in their knee joints. The arthrocenteses were performed under aseptic conditions. Dual-colour FISH analysis was performed using chromosome-7-specific LSI D7S522 (7q31) and chromosome-5-specific LSI EGR1 (5q31)/D5S721 (5p15.2) probes on the slides prepared from synovial fluid of RA patients and controls. Results: The slides of our cases were analysed using two different DNA probes. When the slides hybridised with chromosome-5-specific probes were analysed, no trisomic or monosomic cells were revealed in both patients and controls. However, in eight of 15 patients, trisomy 7 occurred in variable percentages of cells (23% to 48%) of synovial fluid. No monosomic 7 cells were detected in these specimens. All control cases were disomic for chromosome 7. Conclusion: The results of the present investigation suggest that trisomy 7 may play a role in the pathogenesis of synovial hyperproliferation in RA.