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Telomere shortening associated with chromosome instability is arrested in immortal cells which express telomerase activity.
Open accessAbstract
Loss of telomeric DNA during cell proliferation may play a role in ageing and cancer. Since telomeres permit complete replication of eukaryotic chromosomes and protect their ends from recombination, we have measured telomere length, telomerase activity and chromosome rearrangements in human cells before and after transformation with SV40 or Ad5. In all mortal populations, telomeres shortened by approximately 65 bp/generation during the lifespan of the cultures. When transformed cells reached crisis, the length of the telomeric TTAGGG repeats was only approximately 1.5 kbp and many dicentric chromosomes were observed. In immortal cells, telomere length and frequency of dicentric chromosomes stabilized after crisis. Telomerase activity was not detectable in control or extended lifespan populations but was present in immortal populations. These results suggest that chromosomes with short (TTAGGG)n tracts are recombinogenic, critically shortened telomeres may be incompatible with cell proliferation and stabilization of telomere length by telomerase may be required for immortalization.
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“In primary cells deficient for Rb and p53, continued cellular growth beyond the Hayflick limit results in severe telomere shortening, marked genetic instability, and massive cell death—a period referred to as crisis (Counter et al. 1992”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Counter et al. 1992
In the citing paper
“However, as these human fibroblasts undergo additional cell divisions, telomere erosion continues and the loss of telomere capping function produces rampant chromosomal instability and widespread apoptosis, a cellular state termed crisis (27).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [27]
In the citing paper
“Crisis serves as the second checkpoint in tumor suppression and is characterized by multiple chromosomal fusions36.”
From Telomere dysfunction and tumour suppression: the senescence connection (2008) · cites this paper as [36]
In the citing paper
“Telomere maintenance is essential to the replicative potential of malignant cells and the inhibition of telomerase can lead to telomere shortening and cessation of unrestrained proliferation.”
From A highly selective telomerase inhibitor limiting human cancer cell proliferation (2001) · cites this paper as Counter et al., 1992
In the citing paper
“Eventually, telomeres shorten to a critical length and lose their ability to protect the ends of chromosomal DNA (Counter et al., 1992;Blasco et al., 1997).”
From A highly selective telomerase inhibitor limiting human cancer cell proliferation (2001) · cites this paper as Counter et al., 1992
In the citing paper
“Telomere maintenance is essential to the replicative potential of malignant cells and the inhibition of telomerase can lead to telomere shortening and cessation of unrestrained proliferation.”
From A highly selective telomerase inhibitor limiting human cancer cell proliferation (2001) · cites this paper as Counter et al., 1992
In the citing paper
“In cancer cells, the reactivation of telomerase is thought to stabilize telomere length, thereby compensating for the cell division-related telomere erosion and providing unlimited proliferative capacity to malignant cells (Counter et al., 1992;Kim et al., 1994).”
From A highly selective telomerase inhibitor limiting human cancer cell proliferation (2001) · cites this paper as Counter et al., 1992
In the citing paper
“In most normal human cells, telomerase activity is low or not detectable, and telomeric DNA is progressively lost at a rate of 30±120 bp with each replication cycle (Harley et al., 1990;Hastie et al., 1990;Counter et al., 1992).”
From A highly selective telomerase inhibitor limiting human cancer cell proliferation (2001) · cites this paper as Counter et al., 1992
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“Eventually, immortal clonal populations will emerge that can maintain telomere length (Neufeld et al. 1987; Counter et al. 1992).”
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“When telomeres shorten to a critical length, the cell exits the cell cycle, which is characteristic of cell senescence (Counter et al .”
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“The loss of a certain length of the telomere after each cell division gradually diminishes the cell’s division potential and ultimately leads to cell senescence or death [43][7] (chapter 10).”
BackgroundNFX1 Interacts with mSin3A/Histone Deacetylase To Repress hTERT Transcription in Keratinocytes
Xu, M., Luo, W., Elzi, D. J., Grandori, C., & Galloway, D. A. (2008) · Molecular and Cellular Biology · doi:10.1128/mcb.01969-07 · Cited by 74
“Maintenance of telomere length by telomerase is required for sustained cell proliferation, and activation of telomerase is a critical step during cellular immortalization and malignant transformation (7).”
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“maintenance pathway in order to escape crisis, which is only achieved through either 85 reactivation of telomerase found in around 85 - 95 % of cancers, or through elongation of 86 telomeres via the ALT pathway [29-34].”
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“Mammalian telomeres have gained importance because of their possible link with carcinogenesis (15, 17, 27, 63).”
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“In adult humans, most cells, including, but not limited to, ®broblasts (HDF) (Kim et al., 1994), neurons (Kruk et al., 1996), kidney cells (Counter et al., 1992), endothelial cells (Kim et al., 1994), retinal pigment epithelial cells (Bodnar et al., 1998) and human mammary epithelial cells (HMEC)…”
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“This phenomenon can occur in response to a plethora of stressors such as DNA damage, telomere dysfunction [12,13], ionizing radiation [14], high glucose concentrations [15], low-grade inflammation [16] or oxidative stress [17].”
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“However, cells that bypass senescence in this way are still subject to telomeric shortening, continue to age, accumulate chromosomal abnormalities and eventually succumb at a second mortality check point, referred to as crisis (Counter et al., 1992; Girardi et al., 1965).”
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“In contrast, activation of telomerase (Counter et al. 1992; Greider 1998) or inheritance of long telomeres, allows cell immortalization which can predispose to cancer (Stanley and Armanios 2015; McNally et al.”
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“The absence of telomerase activity in most normal human cells results in the progressive shortening of telomeres with each cell division (19, 56, 60), eventuating in growth arrest or replicative senescence (6, 19).”
BackgroundReplicative aging of human articular chondrocytes during ex vivo expansion
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“Without telomeric caps, human chromosomes would undergo end-to-end fusions with formation of dicentric and multicentric chromosomes (Counter et al., 1992; Harley, 1995; Harley et al., 1990; van Steensel et al., 1998).”
BackgroundTelomeres and chromosomal instability
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BackgroundAnalysis of Telomeres and Telomerase
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“Once telomerase is activated, it stabilizes telomere length and permits continued cell division (Counter et al., 1992).”
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“meres to compensate for the progressive loss (5, 6).”
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BackgroundA Critical Role for Pin2/TRF1 in ATM-dependent Regulation
Kishi, S., & Lu, K. P. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m111365200 · Cited by 67
Telomere Crisis, the Driving Force in Cancer Cell Evolution
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“Accordingly, their growth is limited to a certain number of population doublings and comprise a near-exponential growth phase followed by a phase of stagnation (plateau) marked by the absence of net growth (Counter et al. 1992, Harley et al. 1992, Hayflick 1965, Wright & Shay 1992) (Figure 2a).”
BackgroundTelomere dysfunction drives chromosomal instability in human mammary epithelial cells
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“associated with increased numbers of telomere associations, dicentric chromosomes, ring chromosomes, and massive cell death (Counter et al., 1992; Rogan et al., 1995).”
BackgroundA role for WRN in telomere-based DNA damage responses
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“Of significant interest was the finding that telomerase activity resumes in the majority of immortalized cell lines and human tumors (Shay and Bacchetti, 1997) and that telomere array length stabilizes, and in some cases lengthens, in cancerous cells (Counter et al., 1992; Kim et al., 1994).”
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SV40-mediated immortalization of human fibroblasts
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Self-citationTelomere dysfunction and its role in haematological cancer
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“This study identified TLs that were as short as those found in cells undergoing crisis in culture where telomere dysfunction has been shown to drive large-scale genomic rearrangements (Counter et al, 1992; Capper et al, 2007).”
Background
Metadata
- Authors
- Counter, C. M., Avilion, A. A., LeFeuvre, C. E., Stewart, N. G., Greider, C. W., Harley, C. B., & Bacchetti, S.
- Affiliations
- McMaster University (CA)
- Venue
- The EMBO Journal
- Published
- 1992-05-01
- Volume
- 11
- Issue
- 5
- Pages
- 1921-1929
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC556651
- OpenAlex
- W1543500873
- Cited by
- 2,096
- References
- 53
- Citations by year
- 2026: 10 · 2025: 21 · 2024: 25 · 2023: 25 · 2022: 27 · 2021: 35 · 2020: 29 · 2019: 28 · 2018: 39 · 2017: 42 · 2016: 48 · 2015: 53 · 2014: 51 · 2013: 65 · 2012: 55
- FWCI
- 23.80
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Chromosomal and Genetic Variations
- Keywords
- telomere shortening, telomerase, chromosomal instability, cell immortalization, telomere length, dicentric chromosomes, telomeric DNA, SV40 transformation, adenovirus type 5, cell transformation, telomere recombination, cell proliferation, aging, cancer
- MeSH terms
- Cell Transformation, Neoplastic, Cell Transformation, Viral, Chromosomes, Human, DNA, DNA Nucleotidylexotransferase, Humans, Karyotyping, Kidney, Transfection, Telomere, Cellular Senescence
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