title: Decrease of telomeres and increase of interstitial telomeric sites in chromosomes of short-term cultured gastric carcinoma cells detected by fluorescence in situ hybridization.
abstract: BACKGROUND
  Deletion or shortening of chromosomal telomeres is associated with cellular aging and carcinogenesis. Telomeric sites are interstitially located in chromosomes. To clarify the frequency of telomerase abnormalities in cancer and their relationship with any characteristics of gastric carcinomas, telomeric aberrations in eleven cultured specimens of human gastric cancer were investigated by cytogenetic analysis.
  
  
  METHODS
  Chromosomal metaphase specimens, obtained by primary culture of cells from surgical specimens of eleven gastric cancer patients, were examined by fluorescent in situ hybridization (FISH) using all telomeric and chromosome 17 specific-telomeric DNA probes. The number of telomeric signals and interstitial telomeric signals (ITS) were counted. DNA ploidy was examined by flow cytometry.
  
  
  RESULTS
  The mean telomere signal per nucleus (MTS) observed in peripheral blood lymphocytes (PBLs) of normal volunteers (n=10) was 71.3+/-3.9%. The MTS in the carcinoma cells (46.9+/-2.6%) was significantly lower than in PBLs (p<0.01). Although ITS were not observed in PBLs, the mean rate of ITS was 41.2+/-22.0%, and the mean rate of ITS per chromosome was 2.1+/-2.1% in the cancer specimens. In DNA aneuploid carcinoma cells, the MTS was significantly lower, the mean rate of ITS tended to be higher (p=0.072), and the mean rate of ITS per chromosome was significantly higher (p<0.05), than in DNA diploid lymphocytes. Histologically, the mean rate of ITS per chromosome in carcinomas with venous infiltrations was significantly greater than in those without (p<0.05).
  
  
  CONCLUSIONS
  Deletion and interstitial translocation of telomeric loci of chromosomes were frequent alterations in gastric carcinoma cells and increased numbers of interstitial telomeric signals were associated with venous invasion.
authors.affiliation: Division of Surgical Oncology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Kashima
authors.forename: Atsushi
authors.initials: A
authors.lastname: Nanashima
authors.forename: Toru
authors.initials: T
authors.lastname: Yasutake
authors.forename: Terumitsu
authors.initials: T
authors.lastname: Sawai
authors.forename: Takashi
authors.initials: T
authors.lastname: Tsuji
authors.forename: Shigekazu
authors.initials: S
authors.lastname: Hidaka
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Akama
authors.forename: Kousei
authors.initials: K
authors.lastname: Miyashita
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Tagawa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nagayasu
mesh_terms: D000328:Adult; D000368:Aged; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics; D004273:DNA, Neoplasm / Q000235:genetics; D005260:Female; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D008875:Middle Aged; D011003:Ploidies; D013274:Stomach Neoplasms / Q000235:genetics* / Q000473:pathology; D016615:Telomere / Q000235:genetics / Q000378:metabolism*
chemical_list: D004273:DNA, Neoplasm