The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Specific Association of Human Telomerase Activity with Immortal Cells and Cancer
Abstract
Synthesis of DNA at chromosome ends by telomerase may be necessary for indefinite proliferation of human cells. A highly sensitive assay for measuring telomerase activity was developed. In cultured cells representing 18 different human tissues, 98 of 100 immortal and none of 22 mortal populations were positive for telomerase. Similarly, 90 of 101 biopsies representing 12 human tumor types and none of 50 normal somatic tissues were positive. Normal ovaries and testes were positive, but benign tumors such as fibroids were negative. Thus, telomerase appears to be stringently repressed in normal human somatic tissues but reactivated in cancer, where immortal cells are likely required to maintain tumor growth.
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In the citing paper
“Furthermore, although most human cancers (~90%) escape telomere crisis by activating telomerase56, a significant minority of cancers use an alternative telomere maintenance system, referred to as alternative lengthening of telomeres (ALT)161.”
From Telomeres in cancer: tumour suppression and genome instability (2017) · cites this paper as [56]
In the citing paper
“The notion that telomere function may indeed be required for immortalization is supported by the frequent activation of telomerase or ALT in human cancers (Kim et al. 1994; Bryan et al. 1995”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Kim et al. 1994
In the citing paper
“Telomerase activation is observed in approximately 90% of human cancers, irrespective of tumor type, while most normal tissues contain inactivated telomerase.(1)”
From Understanding and exploiting hTERT promoter regulation for diagnosis and treatment of human cancers (2008) · cites this paper as [1]
In the citing paper
“This idea is consistent with the fact that telomerase activity is upregulated in most human cancers, which probably contributes to sustaining their immortality7.”
From The telomere syndromes (2012) · cites this paper as [7]
In the citing paper
“Virally transformed human cells that eliminate p53 and/or pRB function can escape crisis at very low frequencies, and invariably adopt telomere-maintenance programs: 80-90% of human tumors possess some telomerase activity, while the remainder maintain telomeres via a recombination-mediated process termed ALT (for Alternative Lengthening of Telomeres)37-40.”
From Telomere dysfunction and tumour suppression: the senescence connection (2008) · cites this paper as [38]
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 Kim et al., 1994
In the citing paper
“Telomerase, the ribonucleoprotein enzyme maintaining the telomeres of eukaryotic chromosomes, is active in most human cancers and in germline cells but, with few exceptions, not in normal human somatic tissues.”
From A highly selective telomerase inhibitor limiting human cancer cell proliferation (2001) · cites this paper as Kim et al., 1994
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 Kim et al., 1994
In the citing paper
“Telomerase activity has been demonstrated in immortalized cell lines and in 80±90% of human cancer specimens representing a range of cancer types (Counter et al., 1994;Kim et al., 1994;Shay and Bacchetti, 1997)”
From A highly selective telomerase inhibitor limiting human cancer cell proliferation (2001) · cites this paper as Kim et al., 1994
In the citing paper
“Telomerase activity has been found in almost all human tumors but not in adjacent normal cells (3, 4).”
From Inhibition of human telomerase in immortal human cells leads to progressive telomere shortening and cell death (1999) · cites this paper as [3]
In the citing paper
“Over the last decade it has become clear that most human cancers activate telomerase at some point during tumorigenesis, while this activity is largely absent in most normal tissues 70, 71 .”
From The common biology of cancer and ageing (2007) · cites this paper as [70]
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“In earlier reports, telomerase was positive in most of acute leukemia patients, however detailed information about the level of enzyme activity was unknown (Nilsson et al., 1994; Kim et al., 1994).”
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“Kim et al. (5) have described an easy, highly sensitive method for the analysis of telomerase activity. Recent studies (58) have used this method, known as the telomeric repeat amplification protocol (TRAP), to demonstrate that telomerase activity can be detected with a frequency of more than 90% in almost all types o…”
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“Telomerase activity was assessed for all extracts using the TRAP assay [11] according to manufacturers’ protocol (Chemicon), with the following exceptions.”
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“In contrast, highly proliferative cells, such as germ cells and stem cells, as well as 85–95% of cancers express telomerase (9).”
BackgroundInhibition of telomerase activity by cisplatin in human testicular cancer cells
Burger, A. M., Double, J. A., & Newell, D. R. (1997) · European Journal of Cancer · doi:10.1016/s0959-8049(96)00521-7 · Cited by 141
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Cancer and Telomeres—An ALTernative to Telomerase
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“Any of these methods may be complemented by a highly sensitive telomerase activity assay (47, 75), which reveals the extent to which telomerase may or may not be contributing to telomere length maintenance in the tissue of interest.”
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“On the other hand, telomere lengths are maintained in approximately 90% of human cancer cells and immortalized cells by activating telomerase (12).”
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“…repeats (TTAGGG in mammals) to the ends of chromosomes, is undetectable in most diploid, `mortal' cell types and strains (Counter et al., 1992; Kim et al., 1994), but has been observed in a majority of `immortal' cell lines ± aneuploid cells, whether tumor-derived or transformed in vitro,…”
BackgroundMolecular characterization of inter-telomere and intra-telomere mutations in human ALT cells
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“gif" NDATA ITEM> ]> Telomeres in most immortal cell”
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BackgroundPermanent embryo arrest: molecular and cellular concepts
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“The authors would like to thank Dr Pari Basrur for the critical review of this manuscript and for her insightful comments.”
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“mere maintenance and extension of proliferative capacity (Kim et al., 1994).”
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“Although tightly restricted in adult somatic cells under unusual and often neoplastic conditions, telomerase is reactivated in most cancers [54,92,93].”
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“While a majority of human malignancies achieve this by upregulation of telomerase that adds telomere repeats to the chromosomal ends (Kim et al , 1994), a remaining 10 – 15% of human cancers adopt a telomerase-independent mechanism, termed alternative lengthening of telomeres (ALT), to potentiate…”
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“Therein lies the critical importance of our study, since it reveals that three prominent human oncoproteins (HER2/Neu, Ras, and Raf) can transform a telomerase-negative cell to a telomerase-positive cell by activating ER81 and consequently upregulating hTERT expression, as occurs in 90% of all human tumor cells (31, 4…”
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Background
Metadata
- Authors
- Kim, N. W., Piatyszek, M. A., Prowse, K. R., Harley, C. B., West, M. D., Ho, P. L. C., Coviello, G. M., Wright, W. E., Weinrich, S. L., & Shay, J. W.
- Affiliations
- Geron (United States) (US)
- The University of Texas Southwestern Medical Center (US)
- Geron Corporation, Menlo Park, CA 94025.
- Venue
- Science
- Published
- 1994-12-23
- Volume
- 266
- Issue
- 5193
- Pages
- 2011-2015
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2000971601
- Cited by
- 7,091
- References
- 32
- Citations by year
- 2026: 51 · 2025: 104 · 2024: 109 · 2023: 175 · 2022: 140 · 2021: 209 · 2020: 182 · 2019: 181 · 2018: 208 · 2017: 209 · 2016: 235 · 2015: 232 · 2014: 228 · 2013: 222 · 2012: 235
- FWCI
- 85.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r43ca065178-01, 5r01ca050195-05)
- National Institute on Aging (AG07992, R01AG007992)
- National Cancer Institute (CA 50195, CA65178)
- 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
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- telomerase, telomerase activity assay, cellular immortality, cancer, tumor growth, telomere synthesis, benign tumors, cell proliferation
- MeSH terms
- Base Sequence, Cell Division, Cell Line, Cell Line, Transformed, DNA Nucleotidylexotransferase, Enzyme Activation, Enzyme Repression, Female, Humans, Male, Molecular Sequence Data, Neoplasms, Ovary, Testis, Tumor Cells, Cultured, Polymerase Chain Reaction
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