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Cited by 45Telomeres, Telomerase, and SenescenceGenomic variations and chromosomal abnormalitiesChromosomal and Genetic Variations

Telomeric fusions in cultured human fibroblasts as a source of genomic instability

Riboni, Roberta, Casati, Alessandra, Nardo, Tiziana, Zaccaro, Elisabetta, Ferretti, Luca, Nuzzo, Fiorella, Mondello, Chiara·1997·Cancer Genetics and Cytogenetics
DOI 10.1016/s0165-4608(96)00248-8
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Abstract

In a human fibroblast clone we studied the evolution, during culture propagation, of a dicentric chromosome consisting of the end-to-end association of the short arm of chromosome 5 and the long arm of chromosome 16. Dual-color fluorescence in situ hybridization (FISH) with painting probes allowed us to define the structure of a variety of derivative chromosomes and to identify the mechanisms by which they originated. Asymmetric interchanges involving the intercentromeric region of the dicentric, bridge-breakage-fusion events, or breaks followed by sister chromatid fusion, originate unstable hetero- or homodicentric chromosomes with deletion or duplication; breakages not followed by reunion, or intradicentric recombination, presumably originate stable rearranged monocentric chromosomes. The variety of the derivatives is extremely large because the observed events may involve any site of the intercentromeric region, although the majority of them occurs after a break in 16qh. The results of this investigation document the evolution through successive steps of a telomeric fusion, a chromosome anomaly frequently observed in tumor and senescent cells. They also demonstrate that in cultured cells of normal origin, starting with this anomaly, various chromosomal mechanisms may produce translocations, duplications, and deletions. The karyotype instability produced by a telomeric fusion can be relevant for carcinogenesis because it may generate genetic changes critical in the multistep process of transformation.

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  • Genome instability in cells undergoing telomere crisis was initially found to cause aneuploidy, translocations, loss of heterozygosity, and regional amplification through breakage-fusion-bridge cycles.

    “Genome instability in cells undergoing telomere crisis was initially found to give rise to chromosome gains and losses (aneuploidy), translocations, gene loss (manifested as loss of heterozygosity (LOH)) and regional amplification through breakage–fusion–bridge (BFB) cycles1,80,83.”

    From Telomeres in cancer: tumour suppression and genome instability (2017) · cites this paper as [83]

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Authors
Riboni, R., Casati, A., Nardo, T., Zaccaro, E., Ferretti, L., Nuzzo, F., & Mondello, C.
Affiliations
National Research Council (IT)
Corresponding author
Mondello, Chiara
ORCID
Venue
Cancer Genetics and Cytogenetics
Publisher
Elsevier BV
Published
1997-06
Volume
95
Issue
2
Pages
130-136
ISSN
0165-4608 (ISSN-L)
DOI
10.1016/s0165-4608(96)00248-8
OpenAlex
W2048363602
Cited by
45
References
26
Citations by year
2025: 1 · 2022: 3 · 2021: 1 · 2018: 1 · 2017: 2 · 2014: 1 · 2013: 1 · 2012: 1
FWCI
2.03
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Cancer Genetics and Cytogenetics (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
Keywords
telomeric fusions, genomic instability, dicentric chromosomes, chromosome 5, chromosome 16, chromosomal translocation, deletions and duplications, karyotype evolution, carcinogenesis, human fibroblasts
MeSH terms
Cells, Cultured, Chromosome Aberrations, Fibroblasts, Humans, Telomere, In Situ Hybridization, Fluorescence

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