The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
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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TRF1 is degraded by ubiquitin-mediated proteolysis after release from telomeresPreprint
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MethodTelomerase induces immortalization of human esophageal keratinocytes without p16INK4a inactivation.
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Protein Phosphatase 2A Inhibits Nuclear Telomerase Activity in Human Breast Cancer Cells
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BackgroundSelf-citationTelomere attrition and Chk2 activation in human heart failure
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“Telomerase activity is present in human germ line cells and tumor cells (20, 21), but is absent or present at very low levels in most human somatic cells (21, 22).”
BackgroundTelomere biology and age-related diseases
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“Although it is not known if C-strand degradation is a general feature of telomere replication, it is intriguing that human somatic cells lacking telomerase lose telomeric DNA at a rate ∼ 10 times faster than the rate expected from incomplete replication alone (23, 69).”
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Regulation of the human telomerase reverse transcriptase gene
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BackgroundInfluentialHuman arteries engineered in vitro
McKee, J. A., Banik, S. S. R., Boyer, M. J., Hamad, N. M., Lawson, J. H., Niklason, L. E., & Counter, C. M. (2003) · EMBO Reports · doi:10.1038/sj.embor.embor847 · Cited by 184
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MethodSelf-citationN-Terminal Domains of the Human Telomerase Catalytic Subunit Required for Enzyme Activity in Vivo
Armbruster, B. N., Banik, S. S. R., Guo, C., Smith, A. C., & Counter, C. M. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.22.7775-7786.2001 · Cited by 183
“Consistent with low hTERT expression, HA5 cells do not have readily detectable levels of telomerase activity, lose telomeric DNA, and fail to immortalize (12).”
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“…of p53 and pRB by antisense neutralization (Hara et al. 1991) or by viral oncoproteins (Shay et al. 1991) can extend replicative potential, driving further telomere erosion and culminating in a period of massive cell death and rampant chromosomal instability termed crisis (Counter et al. 1992).”
BackgroundInfluentialNew Insights into Nucleolar Architecture and Activity
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ATRX represses alternative lengthening of telomeres
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“After a finite number of additional cell divisions, however, the cells cease proliferation and the culture enters crisis, until a rare cell (approximately 1 in 107 fibroblasts and 1 in 105 epithelial cells) escapes crisis through spontaneous activation of a telomere lengthening mechanism (TLM), and the cell culture be…”
BackgroundPOT1 and TRF2 Cooperate To Maintain Telomeric Integrity
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“Maintenance of the telomeric TTAGGG repeats at human chromosome ends, either by telomerase (13) or by an alternative mechanism (9), is essential for immortalized cells in vitro to escape from the normal limitations of the proliferation capacity.”
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BackgroundResultInfluentialPericentromeric satellite repeat expansions through RNA-derived DNA intermediates in cancer
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“The mechanism underlying HSATII satellite repeat expansion in cancer remains to be defined, but it may involve an RT/ reintegration phenomenon analogous to the phenomenon described for other major repetitive elements, such as LINE-1 (24) and telomeres (25, 26).”
BackgroundAlternative lengthening of telomeres is associated with chromosomal instability in osteosarcomas
Scheel, C., Schaefer, K., Jauch, A. S., Keller, M., Wai, D., Brinkschmidt, C., van Valen, F., Boecker, W., Dockhorn‐Dworniczak, B., & Poremba, C. (2001) · Oncogene · doi:10.1038/sj.onc.1204493 · Cited by 181
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“Human somatic cells gradually lose telomeric sequences as a result of incomplete replication (45).”
BackgroundRadiation-Induced Senescence-like Growth Arrest Requires TP53 Function but not Telomere Shortening
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“Once the TRF progression becomes impaired below 4 kb, cell cycle progression becomes impaired (15, 16).”
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“Crisis is characteristic of cells with massive DNA damage, often, but not exclusively, resulting from telomere dysfunction (Counter et al., 1992; Shay et al., 1993; Lustig, 1999; Chang et al., 2003).”
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“Although human cells lacking pRB and p53 circumvent senescence, most such cells ultimately still cease proliferation through “crisis” due to erosion of telomeres to a critically short length (29).”
BackgroundYashima, K., Litzky, L. A., Kaiser, L. R., Rogers, T. E., Lam, S. C., Wistuba, I. I., Milchgrub, S., Srivastava, S., Piatyszek, M. A., Shay, J. W., et al. (1997) · PubMed · Cited by 175
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“Activation of this enzyme is therefore required for cells to overcome replicative senescence and obtain the ability to divide without limit.(10,11) Studies of the telomerase enzyme complex have revealed the presence of two major subunits contributing to enzymatic activity—a structural RNA component (hTR) that contains…”
BackgroundKyo, S., & Inoue, M. (2002) · Oncogene · doi:10.1038/sj.onc.1205163 · Cited by 180
“Telomerase is a ribonucleoprotein complex that extends andmaintains the telomeres, and activation of this enzyme is therefore required for cells to overcome replicative senescence and obtain the ability to divide without limits (Counter et al., 1992; Greider and Blackburn, 1989).”
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Telomere maintenance by telomerase and by recombination can coexist in human cells
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“Whole-cell extracts were prepared by detergent lysis and assayed by the PCR-based telomere amplification protocol (TRAP; 29) using amounts of protein within the linear range of the assay (0.25 µg for VA13, telomerase-positive derivatives and HeLa cells, and 0.5 µg for HA1-IM cells).”
BackgroundMethodInfluentialThe role of oxidative and nitrosative stress in accelerated aging and major depressive disorder
Maurya, P. K., Noto, C. D. S., Rizzo, L. B., Rios, A. C., Nunes, S. O. V., Barbosa, D. S., Sethi, S., Zeni‐Graiff, M., Mansur, R. B., Maes, M. H. J., et al. (2015) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2015.08.016 · Cited by 174
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Bettin, N., Pegorar, C. O., & Cusanelli, E. (2019) · Cells · doi:10.3390/cells8030246 · Cited by 169
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“Thus, to overcome telomere shortening, immortalized cells invariably regain the ability to maintain telomeres, either through the activation of telomerase activity [16,18] or through the activation of an alternative mechanism that appears to involve recombination [19,20].”
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Lack of cell cycle regulation of telomerase activity in human cells
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Restoration of Telomeres in Human Papillomavirus-Immortalized Human Anogenital Epithelial Cells
Klingelhutz, A. J., Barber, S. A., Smith, P. P., Dyer, K., & McDougall, J. K. (1994) · Molecular and Cellular Biology · doi:10.1128/mcb.14.2.961 · Cited by 167
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Self-citationThe disparity between human cell senescence in vitro and lifelong replication in vivo
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Conserved nucleoprotein structure at the ends of vertebrate and invertebrate chromosomes.
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Regulation of the hTERT telomerase catalytic subunit by the c-Abl tyrosine kinase
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“Telomere shortening in cells continues until crisis and the escape of immortal cells that have reactivated telomerase [14–19].”
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“For analysis of duplications occurring on the q arm subtelomeric region of chromosome 16, cytogenetic analysis was done in five sequential steps, consisting of (1) the protein nucleic acid telomeric probe, (2), the subtelomeric probes, (3) the cosmid probes located adjacent to the integration site, (4) the chromosome…”
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Self-citationTelomerase in the early detection of cancer.
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Regulation and Mechanisms of Mammalian Gene Amplification
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BackgroundIdentification of a nonprocessive telomerase activity from mouse cells.
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Frequent amplification of the telomerase reverse transcriptase gene in human tumors.
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Telomerase as a universal tumor-associated antigen for cancer immunotherapy
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“In contrast, the great majority of human tumors exhibit strong telomerase activity (Kim et al., 1994), express hTERT (Meyerson et al., 1997; Nakamura et al., 1997; Ramakrishnan et al., 1998), and maintain the length of their telomeres (Counter et al., 1992, 1994).”
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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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