Chromosomal fragile sites and relationship between genetic predisposition to small cell lung cancer.


Karadag M., Tunca B., Cecener G., Engeli Ü., Ozyardimci N., Ege E., ...Daha Fazla

Teratogenesis, carcinogenesis, and mutagenesis, cilt.22, sa.1, ss.31-40, 2002 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 22 Sayı: 1
  • Basım Tarihi: 2002
  • Doi Numarası: 10.1002/tcm.1036
  • Dergi Adı: Teratogenesis, carcinogenesis, and mutagenesis
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.31-40
  • Anahtar Kelimeler: small cell lung cancer, chromosome aberration, common fragile sites, genetic pre-disposition, peripheric blood lymphocyte cultures, BREAST-CANCER, SHORT ARM, NONRANDOM DISTRIBUTION, EXPRESSION FREQUENCY, RENAL-CELL, FHIT GENE, HETEROZYGOSITY, APHIDICOLIN, LYMPHOCYTES, SUSCEPTIBILITY
  • Bursa Uludağ Üniversitesi Adresli: Evet

Özet

Fragile sites are non-staining gaps and breaks on mammalian chromosomes. Several investigators have pointed out that these sites may act as factors that predispose to specific chromosomal rearrangements that are present in some cancer cases. The expression of common fragile sites induced by aphidicolin (Ape) was evaluated on prometaphase chromosomes obtained from the peripheral blood lymphocytes of 15 patients with lung cancer, 20 of their clinically healthy family members, and 20 age-matched normal controls. As a result of cytogenetic evaluation carried out by the High Resolution Banding (HRB) technique, 1q21, 2q33, 3p14, 7q32, 13q13, 16q23, 17q21, and 22q12 are defined as fragile sites in patients and relatives. The rate of total fragile sites and 2q33, 3p14, and 16q23 are statistically significant in both patients and relatives when compared with the control group. Therefore, our results showed that common fragile sites might be unstable factors in the human genome and they can be used as suitable markers for genetic predisposition to lung cancer. (C) 2002 Wiley-Liss, Inc.