Gotowe bibliografie tematyczne / Telomeres

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Gotowa bibliografia na temat „Telomeres”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 9 czerwca 2025

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Artykuły w czasopismach na temat "Telomeres"

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Brault, Marie Eve, and Chantal Autexier. "Telomeric recombination induced by dysfunctional telomeres." Molecular Biology of the Cell 22, no. 2 (January 15, 2011): 179–88. http://dx.doi.org/10.1091/mbc.e10-02-0173.

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Telomere maintenance is essential for cellular immortality, and most cancer cells maintain their telomeres through the enzyme telomerase. Telomeres and telomerase represent promising anticancer targets. However, 15% of cancer cells maintain their telomeres through alternative recombination-based mechanisms, and previous analyses showed that recombination-based telomere maintenance can be activated after telomerase inhibition. We determined whether telomeric recombination can also be promoted by telomere dysfunction. We report for the first time that telomeric recombination can be induced in human telomerase-positive cancer cells with dysfunctional telomeres.
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Lin, Chi-Ying, Hsih-Hsuan Chang, Kou-Juey Wu, Shun-Fu Tseng, Chuan-Chuan Lin, Chao-Po Lin та Shu-Chun Teng. "Extrachromosomal Telomeric Circles Contribute to Rad52-, Rad50-, and Polymerase δ-Mediated Telomere-Telomere Recombination in Saccharomyces cerevisiae". Eukaryotic Cell 4, № 2 (лютий 2005): 327–36. http://dx.doi.org/10.1128/ec.4.2.327-336.2005.

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ABSTRACT Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the telomerase reverse transcriptase. In both tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. By using an in vivo inducible Cre-loxP system to generate and trace the fate of marked telomeric DNA-containing rings, the efficiency of telomere-telomere recombination can be determined quantitatively. We show that the telomeric loci are the primary sites at which a marked telomeric ring-containing DNA is observed among wild-type and surviving cells lacking telomerase. Marked telomeric DNAs can be transferred to telomeres and form tandem arrays through Rad52-, Rad50-, and polymerase δ-mediated recombination. Moreover, increases of extrachromosomal telomeric and Y′ rings were observed in telomerase-deficient cells. These results imply that telomeres can use looped-out telomeric rings to promote telomere-telomere recombination in telomerase-deficient Saccharomyces cerevisiae.
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Bechard, Laura H., Bilge D. Butuner, George J. Peterson, Will McRae, Zeki Topcu, and Michael J. McEachern. "Mutant Telomeric Repeats in Yeast Can Disrupt the Negative Regulation of Recombination-Mediated Telomere Maintenance and Create an Alternative Lengthening of Telomeres-Like Phenotype." Molecular and Cellular Biology 29, no. 3 (November 24, 2008): 626–39. http://dx.doi.org/10.1128/mcb.00423-08.

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ABSTRACT Some human cancers maintain telomeres using alternative lengthening of telomeres (ALT), a process thought to be due to recombination. In Kluyveromyces lactis mutants lacking telomerase, recombinational telomere elongation (RTE) is induced at short telomeres but is suppressed once telomeres are moderately elongated by RTE. Recent work has shown that certain telomere capping defects can trigger a different type of RTE that results in much more extensive telomere elongation that is reminiscent of human ALT cells. In this study, we generated telomeres composed of either of two types of mutant telomeric repeats, Acc and SnaB, that each alter the binding site for the telomeric protein Rap1. We show here that arrays of both types of mutant repeats present basally on a telomere were defective in negatively regulating telomere length in the presence of telomerase. Similarly, when each type of mutant repeat was spread to all chromosome ends in cells lacking telomerase, they led to the formation of telomeres produced by RTE that were much longer than those seen in cells with only wild-type telomeric repeats. The Acc repeats produced the more severe defect in both types of telomere maintenance, consistent with their more severe Rap1 binding defect. Curiously, although telomerase deletion mutants with telomeres composed of Acc repeats invariably showed extreme telomere elongation, they often also initially showed persistent very short telomeres with few or no Acc repeats. We suggest that these result from futile cycles of recombinational elongation and truncation of the Acc repeats from the telomeres. The presence of extensive 3′ overhangs at mutant telomeres suggests that Rap1 may normally be involved in controlling 5′ end degradation.
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Kondratieva, Yu A., and L. P. Mendeleeva. "Characteristics of telomere length in patients with hematological diseases (literature review)." Oncohematology 16, no. 1 (April 14, 2021): 23–30. http://dx.doi.org/10.17650/1818-8346-2021-16-1-23-30.

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Telomeres are protein structures that regulate the process of cellular aging and play the role of a protective “cap” on the end sections of chromosomes. The telomeres of nucleated cells undergo permanent shortening during their lifetime as a result of multiple cycles of DNA replication. The enzyme that provides completion of the missing telomeric repeats at the ends of chromosomes is called “telomerase”. However, recovery of critically short telomeres by telomerase or recombination in somatic cells is limited due to the presence of a large accumulation of unclosed telomeres, which triggers apoptosis. The death of stem cells due to telomere depletion ensures the selection of abnormal cells in which the genome instability contributes to malignant progression. During carcinogenesis, cells acquire mechanisms for maintaining telomeres in order to avoid programmed death. In addition, tumor cells are able to support the telomere's DNA, counteracting its shortening and premature death. Activation of telomere length maintenance mechanisms is a hallmark of most types of cancers. In the modern world, there is an increasing interest in studying the biological characteristics of telomeres. The development of new methods for measuring telomere length has provided numerous studies to understand the relationship between telomere length of human nucleated cells and cancer. Perhaps maintaining telomere length will be an important step, determining the course and prognosis of the disease. The purpose of this review is to provide an analysis of published data of the role and significance of telomere length in patients with hematological malignancies.
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Basenko, Evelina, Zeki Topcu, and Michael J. McEachern. "Recombination Can either Help Maintain Very Short Telomeres or Generate Longer Telomeres in Yeast Cells with Weak Telomerase Activity." Eukaryotic Cell 10, no. 8 (June 10, 2011): 1131–42. http://dx.doi.org/10.1128/ec.05079-11.

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ABSTRACT Yeast mutants lacking telomerase are able to elongate their telomeres through processes involving homologous recombination. In this study, we investigated telomeric recombination in several mutants that normally maintain very short telomeres due to the presence of a partially functional telomerase. The abnormal colony morphology present in some mutants was correlated with especially short average telomere length and with a requirement for RAD52 for indefinite growth. Better-growing derivatives of some of the mutants were occasionally observed and were found to have substantially elongated telomeres. These telomeres were composed of alternating patterns of mutationally tagged telomeric repeats and wild-type repeats, an outcome consistent with amplification occurring via recombination rather than telomerase. Our results suggest that recombination at telomeres can produce two distinct outcomes in the mutants we studied. In occasional cells, recombination generates substantially longer telomeres, apparently through the roll-and-spread mechanism. However, in most cells, recombination appears limited to helping to maintain very short telomeres. The latter outcome likely represents a simplified form of recombinational telomere maintenance that is independent of the generation and copying of telomeric circles.
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Cook, Brandoch D., Jasmin N. Dynek, William Chang, Grigoriy Shostak, and Susan Smith. "Role for the Related Poly(ADP-Ribose) Polymerases Tankyrase 1 and 2 at Human Telomeres." Molecular and Cellular Biology 22, no. 1 (January 1, 2002): 332–42. http://dx.doi.org/10.1128/mcb.22.1.332-342.2002.

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ABSTRACT Telomere maintenance is essential for the continuous growth of tumor cells. In most human tumors telomeres are maintained by telomerase, a specialized reverse transcriptase. Tankyrase 1, a human telomeric poly(ADP-ribose) polymerase (PARP), positively regulates telomere length through its interaction with TRF1, a telomeric DNA-binding protein. Tankyrase 1 ADP-ribosylates TRF1, inhibiting its binding to telomeric DNA. Overexpression of tankyrase 1 in the nucleus promotes telomere elongation, suggesting that tankyrase 1 regulates access of telomerase to the telomeric complex. The recent identification of a closely related homolog of tankyrase 1, tankyrase 2, opens the possibility for a second PARP at telomeres. We therefore sought to establish the role of tankyrase 1 at telomeres and to determine if tankyrase 2 might have a telomeric function. We show that endogenous tankyrase 1 is a component of the human telomeric complex. We demonstrate that telomere elongation by tankyrase 1 requires the catalytic activity of the PARP domain and does not occur in telomerase-negative primary human cells. To investigate a potential role for tankyrase 2 at telomeres, recombinant tankyrase 2 was subjected to an in vitro PARP assay. Tankyrase 2 poly(ADP-ribosyl)ated itself and TRF1. Overexpression of tankyrase 2 in the nucleus released endogenous TRF1 from telomeres. These findings establish tankyrase 2 as a bona fide PARP, with itself and TRF1 as acceptors of ADP-ribosylation, and suggest the possibility of a role for tankyrase 2 at telomeres.
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Perera, Omesha N., Alexander P. Sobinoff, Erdahl T. Teber, Ashley Harman, Michelle F. Maritz, Sile F. Yang, Hilda A. Pickett, et al. "Telomerase promotes formation of a telomere protective complex in cancer cells." Science Advances 5, no. 10 (October 2019): eaav4409. http://dx.doi.org/10.1126/sciadv.aav4409.

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Telomerase is a ribonucleoprotein complex that catalyzes addition of telomeric DNA repeats to maintain telomeres in replicating cells. Here, we demonstrate that the telomerase protein hTERT performs an additional role at telomeres that is independent of telomerase catalytic activity yet essential for telomere integrity and cell proliferation. Short-term depletion of endogenous hTERT reduced the levels of heat shock protein 70 (Hsp70-1) and the telomere protective protein Apollo at telomeres, and induced telomere deprotection and cell cycle arrest, in the absence of telomere shortening. Short-term expression of hTERT promoted colocalization of Hsp70-1 with telomeres and Apollo and reduced numbers of deprotected telomeres, in a manner independent of telomerase catalytic activity. These data reveal a previously unidentified noncanonical function of hTERT that promotes formation of a telomere protective complex containing Hsp70-1 and Apollo and is essential for sustained proliferation of telomerase-positive cancer cells, likely contributing to the known cancer-promoting effects of both hTERT and Hsp70-1.
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Chan, Simon R. W. L., and Elizabeth H. Blackburn. "Telomeres and telomerase." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (January 29, 2004): 109–22. http://dx.doi.org/10.1098/rstb.2003.1370.

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Telomeres are the protective DNA–protein complexes found at the ends of eukaryotic chromosomes. Telomeric DNA consists of tandem repeats of a simple, often G–rich, sequence specified by the action of telomerase, and complete replication of telomeric DNA requires telomerase. Telomerase is a specialized cellular ribonucleoprotein reverse transcriptase. By copying a short template sequence within its intrinsic RNA moiety, telomerase synthesizes the telomeric DNA strand running 5' to 3' towards the distal end of the chromosome, thus extending it. Fusion of a telomere, either with another telomere or with a broken DNA end, generally constitutes a catastrophic event for genomic stability. Telomerase acts to prevent such fusions. The molecular consequences of telomere failure, and the molecular contributors to telomere function, with an emphasis on telomerase, are discussed here.
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Dreesen, Oliver, and George A. M. Cross. "Telomerase-Independent Stabilization of Short Telomeres in Trypanosoma brucei." Molecular and Cellular Biology 26, no. 13 (July 1, 2006): 4911–19. http://dx.doi.org/10.1128/mcb.00212-06.

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ABSTRACT In cancer cells and germ cells, shortening of chromosome ends is prevented by telomerase. Telomerase-deficient cells have a replicative life span, after which they enter senescence. Senescent cells can give rise to survivors that maintain chromosome ends through recombination-based amplification of telomeric or subtelomeric repeats. We found that in Trypanosoma brucei, critically short telomeres are stable in the absence of telomerase. Telomere stabilization ensured genomic integrity and could have implications for telomere maintenance in human telomerase-deficient cells. Cloning and sequencing revealed 7 to 27 TTAGGG repeats on stabilized telomeres and no changes in the subtelomeric region. Clones with short telomeres were used to study telomere elongation dynamics, which differed dramatically at transcriptionally active and silent telomeres, after restoration of telomerase. We propose that transcription makes the termini of short telomeres accessible for rapid elongation by telomerase and that telomere elongation in T. brucei is not regulated by a protein-counting mechanism. Many minichromosomes were lost after long-term culture in the absence of telomerase, which may reflect their different mitotic segregation properties.
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Kishtagari, Ashwin, and Justin Watts. "Biological and clinical implications of telomere dysfunction in myeloid malignancies." Therapeutic Advances in Hematology 8, no. 11 (October 6, 2017): 317–26. http://dx.doi.org/10.1177/2040620717731549.

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Telomeres at the ends of linear chromosomes protect the genome. Telomeres shorten with each round of cell division, placing a finite limit on cell growth. Telomere attrition is associated with cell senescence and apoptosis. Telomerase, a specialized ribonucleoprotein complex, maintains telomeres homeostasis through repeat addition of telomere sequences to the 3′ telomeric overhang. Telomere biology is closely related to cancer and normal aging. Upregulation of telomerase or activation of the alternative pathway of telomere lengthening is a hallmark of cancer cells, making telomerase an attractive target for cancer therapeutics. In this review, we will discuss telomere biology and the prognostic implications of telomere length in acute myeloid leukemia, and review exciting new investigational approaches using telomerase inhibitors in acute myeloid leukemia and other myeloid malignancies.
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Rozprawy doktorskie na temat "Telomeres"

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Shakirov, Yevgeniy Vitalievich. "Telomeres and telomere binding proteins in Arabidopsis thaliana." Diss., Texas A&M University, 2004. http://hdl.handle.net/1969.1/422.

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Telomeres are important protein-DNA structures at the ends of linear eukaryotic chromosomes that are necessary to prevent chromosome fusions and exonuclease attack. We found that telomere tracts in Arabidopsis are fairly uniformly distributed throughout a size range of 2-9kb. Unexpectedly, telomeres in WS plants displayed a bimodal size distribution with some individuals exhibiting 4-8 kb telomeres and others 2-5 kb telomeres. We also examined the dynamics of telomere tracts on individual chromosome ends. Following the fate of telomeres in plants through successive generations, we found that the shortest telomeres were typically elongated in the subsequent generation, while the longest telomeres were usually shortened. Thus, telomere length homoeostasis is achieved through intermittent telomerase action on shorter telomeres to attain an optimal size.Single-strand telomere binding proteins were also analyzed. Four major telomere binding protein complexes from cauliflower were identified and their DNA-binding properties characterized. The DNA-binding component of one of the complexes was purified and analyzed by mass-spectrometry. Peptide mass data was used to search for putative protein candidates from the Arabidopsis thaliana database. Additionally, two Arabidopsis genes, AtPot1 and AtPot2, were identified and characterized. The genes encode two single-strand telomeric DNA binding proteins. AtPot1 and AtPot2 proteins can homo- and heterodimerize in vitro. Pot1 protein predominantly localizes to the nucleolus, whereas Pot2 is exclusively nuclear. Plants over-expressing full-length Pot1 and Pot2 proteins had no obvious phenotype, while over-expression of P2DBD and P1∆DBD caused moderate telomere shortening. Plants over-expressing P2DBD had severe morphological and reproductive defects, multiple chromosome abnormalities and aneuploidy. Over-expression of a chimeric protein DBD-P1∆DBD led to rapid telomere shortening, confirming the involvement of Arabidopsis Pot proteins in telomere length maintenance. Intriguingly, telomerase in DBD-P1∆DBD-EYFP plants is inactivated, suggesting that Pot proteins are also involved in regulation of telomerase activity. The analysis of Arabidopsis telomeres and telomere binding proteins will provide additional information towards understanding the role of the telomeric nucleoprotein complex in eukaryotic chromosome biology.
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Maddison, Rachelle Louise. "Telomeres in the absence of telomerase in Saccharomyces cerevisiae." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/30365.

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The aim of this study was to screen a list of proteins which were suggested to have roles in telomerase-independent telomere maintenance. Of the proteins screened some had no effect on post-senescent survival (Nup53p and Crp1p). Other proteins are suggested to function in post-senescent survival (M1p1p, M1p2p, Dhh1p, Rrm3p and Stm1p).;The importance of the affect of the chromatin context on post-senescent survival was identified with proteins involved in chromatin remodelling (Chd1p, Isw1p and Isw2p) and modifying (Rdp3p) identified as also affecting survival. Of particular interest was the strain dependency of their effects, with opposing roles in post-senescent survival in the YP1 and Y55 strains. More work is needed to fully characterise these roles. Their effects on post-senescent survival could be by them directly affecting the telomeric and subtelomeric chromatin or by indirectly affecting the chromatin of the rest of the genome, and hence the transcription of other genes involved in post-senescent survival.;In agreement with previous studies a role for Exo1p in post-senescent survival was identified. In addition the other RAD2 family members (Rad27p, Rad2p, Din7p and Yen1p) were also found to be involved in post-senescent survival. The RAD2 family members are involved in either inhibiting Type I or promoting Type II survival mechanisms immediately following senescence. The data is also suggestive of a role for the family in maintaining post-senescent survival.
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Moye, Aaron Lavel. "Understanding the relationship between telomeres, telomerase, and DNA G-quadruplexes." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17713.

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Cancer cells elongate their telomeres - G-rich repetitive sequences found at the end of linear chromosomes, allowing limitless replicative potential in these cells. Approximately 85% of cancers use telomerase to extend telomeres, making it an attractive potential anti-cancer target. The G-rich nature of telomeres allows the formation of DNA G-quadruplex secondary structures. Previous data had demonstrated that telomeric G-quadruplex substrates could not be extended by ciliate telomerase (Zahler et al., 1991). However, while the above observation is true for anti-parallel G-quadruplexes, parallel G-quadruplexes were shown to be substrates for ciliate telomerase (Oganesian et al., 2006). Whether human telomerase could extend parallel G-quadruplexes was unknown. In this thesis, I confirmed that human telomerase, like ciliate telomerase, can extend parallel, intermolecular G-quadruplexes in vitro. The ability of telomerase to extend G-quadruplexes is also true for parallel, intramolecular G-quadruplexes, indicating that the parallel nature of the structure allows telomerase extension. Extension of parallel G-quadruplexes using both biochemical and single-molecule FRET microscopy revealed that parallel G-quadruplexes are bound by telomerase as a distinct substrate and partially unfolded, allowing hybridisation of the RNA template. This partially unwound G-quadruplex is extended by human telomerase to the hTR template boundary, followed by translocation and complete G-quadruplex unfolding. Stabilisation of the parallel G-quadruplex using a parallel-G-quadruplex-specific ligand NMM did not inhibit telomerase activity demonstrating that chemically-stabilised parallel G-quadruplexes can be extended by human telomerase. Using a G-quadruplex specific antibody I showed that G-quadruplexes at telomeres increased after NMM treatment, indicating that parallel G-quadruplexes exist at human telomeres in vivo, and that telomeres with G-quadruplexes are a site of localisation for human telomerase. A potential protective effect of Gquadruplexes at uncapped telomeres was also investigated. In Saccharomyces cerevisiae lacking cdc13, equivalent in function to mammalian POT1, the DNA damage response could be suppressed by stabilising Gquadruplexes, showing that G-quadruplexes can have a protective effect at uncapped telomeres, but whether this is true at mammalian telomeres was unknown. In chapter 3 of this thesis I demonstrated that the DNA damage response at uncapped telomeres was suppressed by G-quadruplex stabilising ligands in G1 cells. I showed that G-quadruplex-telomere colocalisation increase in the absence of POT1, consistent with in vitro FRET experiments (Hwang et al., 2012). Treatment of POT1-deficient telomeres in G1 with G-quadruplex stabilising ligands reduced G-quadruplex-telomeres colocalisation. I provide preliminary data indicating that the nucleotide excision repair pathway is responsible for this phenotype, and that loss of stabilised telomeric G-quadruplexes is linked to the DNA damage response suppression phenotype. This thesis provides a body of work that improves our understanding of the role of G-quadruplexes at telomeres.
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Lee, Joyce Hiu Yan. "Detection of Alternative Lengthening of Telomeres in Telomerase-Positive Cancers." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17252.

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Immortalisation is a hallmark of cancer and requires activation of a telomere lengthening mechanism (TLM) to counteract natural telomere shortening. There are two TLMs: telomerase, reported in 85% of cancers, and Alternative Lengthening of Telomeres (ALT), reported in 13% of cancers. Because most somatic tissues do not have TLM activity, TLMs are widely regarded as targets for the development of anti-cancer therapies. Preliminary data from the Reddel laboratory indicated that in non-small cell lung carcinoma (NSCLC), ALT was more common than previously reported but mostly at very low levels, and together with telomerase activity. A panel of NSCLCs were examined for ALT and telomerase activity by the C-Circle Assay (CCA) and TRAP assay, respectively. ALT (at least a low level) and telomerase coexisted in 18% of the panel, suggesting that ALT is a more important therapeutic target in NSCLC than previously appreciated. ALT+/telomerase+ tumours could result from intratumoral heterogeneity, or from individual cancer cells being dual-positive. It was hypothesised that ALT and telomerase may be activated spontaneously in the same cancer cell. As functional studies are not possible in human tumours, a panel of 384 cancer cell lines was examined to determine whether some telomerase+ lines have ALT markers. Three cell lines positive for CCA and TRAP activity were subcloned, each of which were positive for both TLMs, indicating that both TLMs may occur spontaneously in a cancer cell. One of the dual-positive lines (LOX IMVI) was used for functional studies. A DNA tag inserted into one of its telomeres was copied on to other telomeres; this is regarded as the most definitive empirical evidence for the presence of a functional ALT mechanism. Therefore, telomere lengthening is occurring via ALT activity. The functional significance of telomerase activity was also addressed by CRISPR/Cas9-mediated knockout of the TERC gene. A blood-based diagnostic for ALT could be important for patient management and could be provided by the CCA because C-Circles have been reported in the blood of patients with ALT+ osteosarcomas. It was demonstrated that C-Circles are secreted by cancer cells in vesicles, which may be lost during plasma isolation. This knowledge may allow correct implementation of the CCA as a blood-based diagnostic for ALT activity.
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Lee, Michael. "Next Generation Sequencing Strategies to Investigate Telomeres in Cancer." Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21844.

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Telomeres are regions of repetitive DNA at the ends of human chromosomes that function to maintan the integrity of the genome. Telomere attrition is associated with celluar ageing, whilst telomere maintenance is a prerequisite for replicative immortality in cancer. There are two telomere maintenance mechanisms (TMM) that cancer cells can utilize, the enzyme telomerase, or the Alternative Lengthening of Telomeres (ALT) pathway. These two mechanisms synthesise telomeres in very distinct ways leading to differences in their telomere sequence composition and length. The molecular pathways involved with the selective activation of one TMM over the other remain unclear. In the last decade, whole genome sequencing (WGS) has proven to be an invaluable tool for the study of cancer, leading to the discovery of novel gene mutations that either drive the disease or confer an increased risk of developing it. The utility of this technique has led to the creation of vast cancer WGS data resources, in particular The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC), that are available for cancer researchers worldwide to use. This provides an excellent resource from which we can better understand and associate genetic markers and telomere sequence content across cancers, as well as between tumours that utilise the telomere maintenance mechanisms telomerase and ALT. In order to utilise these available datasets, we require a WGS‐based approach to determine the TMM status of a tumour, as experimental validation requires obtaining cellular material. We propose that differences exist in telomere sequence composition and length between ALT and telomerase cancers that can be used to determine the TMM status of a tumour from WGS data. In this thesis, we first compared a range of WGS‐based telomere content measurement tools against the lab‐based technique q‐PCR, in order to assess their accuracy in quantitating telomere content, whilst simultaneously enriching for variant telomeric sequences. We then applied the best of these tools to two experimentally validated tumour datasets, pancreatic neuroendocrine tumours and melanomas, in order to directly analyse and compare the telomere sequence content between tumours that utilise ALT and those that do not. Finally, we exploited the differences in telomere sequence content in order to develop a classifier capable of determining the ALT status of a tumour from WGS data, and applied it to WGS data from 821 TCGA tumours, to identify the molecular pathways associated with the activation of ALT. We were able to demonstate that WGS‐based telomere content measurement tools perform well, producing comparable results to q‐PCR, with R2 = 0.9516. We have developed a methodology for the accuracte quantification of variant repeats within telomere sequences, identifying a number of differences in telomere sequence composition between ALT positive (+ve) and ALT negative (‐ve) tumours. We have demonstated the utility of this methodology to develop a WGS‐based classifier capable of predicting the ALT status of a tumour with 91.6% accuracy. Analysis of pathway mutations that were under‐represented in ALT tumours, across 1,075 tumour samples, revealed that the autophagy, cell cycle control of chromosomal replication, and transcriptional regulatory network in embryonic stem cells pathways were involved in the survival of ALT tumours. Overall, we have demonstrated the capability and utility of WGS to investigate telomere sequence content, shown how telomere sequence content can be used to stratify cancers by TMM, and applied this to cancer WGS datasets to elucidate the genetic changes that associate with each TMM. This thesis provides a useful resource for future studies seeking to investigate the role of telomere sequence content in disease and overall health.
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Sherwood, Rebecca. "The Effect of the Copy Number of the Telomerase RNA Gene on the Elongation of Telomeres in Saccharomyces cerevisiae." Thesis, Boston College, 2008. http://hdl.handle.net/2345/532.

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Thesis advisor: Clare O'Connor<br>Telomeres are repeated sequences at the ends of chromosomes, which promote chromosome stability by preventing the loss of necessary nucleotides from the DNA with successive rounds of replication. Telomeres are elongated by the enzyme telomerase, which has both a protein component and an RNA component. In the yeast Saccharomyces cerevisiae, the TLC1 gene encodes the RNA component of the enzyme. Telomerase RNA interacts with several proteins to perform its function, including the Ku protein, which binds to the end of the DNA and helps to recruit telomerase to the chromosome thereby facilitating the lengthening of chromosome ends. Ku interacts with telomerase RNA at the site of a 48-nucleotide stem-loop on the RNA's structure. Previous experiments have shown that yeast strains engineered to carry two copies of the TLCI gene exhibit higher levels of telomerase RNA than those that have only one copy of the gene. Also, a yeast strain carrying a copy of the mutant tlc1Δ48 gene, which contains a deletion of the 48-nucleotide stem-loop, contains lower levels of telomerase RNA than a strain with the wild type TLC1 gene. This series of experiments is investigating whether the copy number of the telomerase RNA gene affects the elongation of telomeres in S. cerevisiae. In order to determine this effect, the de novo telomere addition of four strains was examined, as were the native telomere lengths of these strains. The assay indicated that the efficiency of telomere elongation was unchanged by increasing the copy number of the wild type gene but was increased upon increasing the copy number of the mutant gene. Analysis of the native telomere lengths showed that increasing the copy number of either the wild type or the mutant gene allowed the cells to maintain their telomeres at a longer length<br>Thesis (BS) — Boston College, 2008<br>Submitted to: Boston College. College of Arts and Sciences<br>Discipline: Biology<br>Discipline: College Honors Program
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Schuller, Christine Children's Cancer Institute Australia for Medical Research Faculty of Medicine UNSW. "Telomeres and telomerase in haematopoietic progenitors and bone marrow endothelial cells." Publisher:University of New South Wales. Children's Cancer Institute Australia for Medical Research, 2008. http://handle.unsw.edu.au/1959.4/41098.

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In normal human somatic cells, the length of telomeres (chromosomal end structures) decreases with each cell division until reaching a critically short length, which halts cell proliferation and induces senescence. The enzyme telomerase, which functions to maintain telomeres at a length that is permissive for cell division, is expressed in approximately 85% of cancer cells and some stem and progenitor cells, including haematopoietic progenitor cells (HPCs), but not most other normal somatic cells. Previous investigations have demonstrated that ectopic expression of telomerase reverse transcriptase (hTERT) reconstitutes telomerase activity, resulting in telomere elongation in some normal human cell types. However, similar experiments performed in HPCs and endothelial cells have demonstrated a dissociation between the expression of telomerase activity and telomere lengthening. This thesis is focussed on further investigating telomerase-mediated telomere length regulation in HPCs and endothelial cells. Short telomeres in bone marrow and blood leukocytes are associated with the development of disorders linked to bone marrow failure. However, to date a relationship between telomere length and myeloid cell proliferative potential has not been demonstrated. In the current investigations, the telomere length and proliferative potential of 31 cord blood-derived HPCs was determined. Regression analysis revealed a significant correlation between mean telomere length and erythroid cell expansion, but not expansion of other myeloid lineage cells. Another novel finding was that telomerase activity was upregulated in lineage-committed CD34- erythroid cells that were positive for the erythroid-specific lineage marker glycophorin A. It was also functionally demonstrated that telomerase activity facilitates the maximum expansion of erythroid cells. To address the dissociation between telomerase activity and telomere maintenance in BMECs, a dominant negative mutant of the telomere binding protein TRF1, which functions to regulate telomere accessibility, was over-expressed in hTERT-transduced BMECs. These studies showed that telomere access, as well as oncogene expression and exposure to oxidative stress, contribute to telomere length regulation in BMECs. Overall, the results from these investigations demonstrate for the first time the functional significance of telomere length and telomerase activity in ex vivo expansion of erythroid cells, and provide novel insight to the molecular complexity of telomere length maintenance in endothelial cells.
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8

Henson, Jeremy D. "The role of Alternative Lengthening of Telomeres in human cancer." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/1533.

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Activation of a telomere maintenance mechanism is a vital step in the development of most cancers and provides a target for the selective killing of cancer cells. Cancers can use either telomerase or Alternative Lengthening of Telomeres (ALT) to maintain their telomeres and inhibition of either telomere maintenance mechanism can cause cancer cells to undergo senescence or apoptosis. Although telomerase inhibitors are undergoing clinical trials, on commencing this study very little was known about the role of ALT in cancer, what proteins were involved in its mechanism and regulation and how it could be targeted clinically. The primary aim of this thesis was to develop an assay for ALT suitable for examining archived tumour specimens and to begin using it to examine the prevalence and clinical significance of ALT in cancer. This assay and gene expression analysis was also used to identify genes that are involved in or associated with the activation of the ALT mechanism, to contribute towards the overall goal of an ALT cancer therapy. The ALT mechanism involves recombination mediated replication and ALT cells have a marked increase in a range of recombinational events specifically at their telomeres. Presumably, as a consequence of this the telomere lengths of ALT cells are very heterogeneous and on average long. This can be detected by terminal restriction fragment (TRF) Southern analysis, which has been used previously as the definitive test for ALT activity. However, TRF analysis requires intact genomic DNA and is unsuitable for tumour specimens which are commonly archived by paraffin embedding. Another hallmark of ALT is ALT-associated PML bodies (APBs) which are the subset of PML bodies that contain telomeric DNA. Work done in this study to consolidate APBs as a hallmark of ALT, combined with published data, showed 29/31 ALT[+], 3/31 telomerase[+] and 0/10 mortal cell lines/strains are APB[+]. The three APB[+]/telomerase[+] cell lines identified here had an order of magnitude lower frequency of APB[+] nuclei than the ALT[+] cell lines. APBs may be functionally linked to the ALT mechanism and contain the recombination proteins that are thought to be involved in the ALT mechanism. This study, in collaboration with Dr W-Q Jiang, strengthened this functional link by demonstrating that loss of ALT activity (as determined by TRF analysis) coincided with the disruption of APBs. The detection of APBs was developed into a robust assay for ALT in archived tumour specimens using a technique of combined immunofluorescence and telomere fluorescence in situ hybridisation. It was demonstrated that the APB assay concurred exactly with the standard assay for ALT (TRF analysis) in 60 tumours for which TRF analysis gave unequivocal results. The APB assay may be a more appropriate technique in the case of tumour specimen heterogeneity, which may explain why the APB assay was able to give definitive results when TRF analysis was equivocal. We demonstrated that intratumoral heterogeneity for ALT does exist and this could explain why about 3% of tumours in this study were APB[+] but with more than a ten-fold reduction in the frequency of APB[+] nuclei. This study also made the novel discovery of single stranded C-rich telomeric DNA inside APBs which potentially could be used to make the APB assay more suitable for routine pathology laboratory use. The APB assay was used to show that ALT is a significant concern for oncology. ALT was utilised in approximately one quarter of glioblastoma multiforme (GBM), one third of soft tissue sarcomas (STS) including three quarters of malignant fibrous histiocytomas (MFH), half of osteosarcomas and one tenth of non-small cell lung carcinomas (NSCLC). Furthermore, the patients with these ALT[+] tumours had poor survival; median survivals were 2 years for ALT[+] GBM, 4 years for ALT[+] STS including 3.5 years for ALT[+] MFH and 5 years for ALT[+] osteosarcoma. ALT[+] STS and osteosarcomas were also just as aggressive as their ALT[-] counterparts in terms of grade and patient outcome. ALT status was not found to be associated with response to chemotherapy in osteosarcomas or survival in STS. ALT was however, less prevalent in metastatic STS. The APB assay was a prognostic indicator for GBM and was correlated with three fold increased median survival in GBM (although this survival was still poor). ALT was more common in lower grade astrocytomas (88% ALT[+]) than GBM (24% ALT[+]) and ALT[+] GBM had an identical median age at diagnosis to that reported for secondary GBM. It is discussed that these data indicate that ALT was indirectly associated with secondary GBM and is possibly an early event in its progression from lower grade astrocytoma. This is relevant because secondary GBM have distinct genetic alterations that may facilitate activation of the ALT mechanism. Putative repressors of ALT could explain why this study found that ALT varied among the different STS subtypes. ALT was common in MFH (77%), leiomyosarcoma (62%) and liposarcoma (33%) but rare in rhabdomyosarcoma (6%) and synovial sarcoma (9%). ALT was not found in colorectal carcinoma (0/31) or thyroid papillary carcinoma (0/17) which have a high prevalence of telomerase activity and a reduced need for a telomere maintenance mechanism (low cell turnover), respectively. A yeast model of ALT predicts that one of the five human RecQ helicases may be required for ALT. Using the APB assay to test for the presence of ALT in tumours from patients with known mutations in either WRN or RECQL4 it was demonstrated that neither of these RecQ helicases is essential for ALT. Although p53 and mismatch repair (MMR) proteins have been suggested to be possible repressors of ALT, there was no apparent increase in the frequency of ALT in tumours from patients with a germline mutation in p53 codon 273 or in colorectal carcinomas that had microsatellite instability and thus MMR deficiency. Also contrary to being a repressor of ALT but consistent with its ability to interact with a protein involved in the ALT mechanism, the MMR protein MLH1, was demonstrated to be present in the APBs of an ALT[+] cell line. To further test for genes that may be involved in the ALT mechanism or associated with its activation, RNA microarray was used to compare the gene expression of 12 ALT[+] with 12 matched telomerase[+] cell lines; 240 genes were identified that were significantly differentially expressed (p<0.005) between the ALT[+] and telomerase[+] cell lines. Only DRG2 and SFNX4 were significantly differentially expressed after adjusting for the estimated false positive rate. Overall, DRG2, MGMT and SATB1 were identified as most likely to be relevant to the ALT[+] tumours and Western analysis indicated that DRG2 and MGMT levels were down-regulated after activation of ALT and up-regulated after activation of telomerase, whereas SATB1 protein levels appeared to be up-regulated after immortalisation but to a higher degree with activation of ALT compared to telomerase. Since lack of MGMT is known to be a determinant of temozolomide sensitivity in GBM, the possibility that ALT and the APB assay could be used to predict temozolomide sensitivity is discussed. The microarray data was consistent with MGMT expression being suppressed by EGF (p < 0.05), indicating that caution may be needed with combining EGFR inhibitors with temozolomide in ALT cancers. One ALT[+] cell line which did not express MGMT had TTAA sequence in its telomeres. This could possibly have resulted from mutations due to lack of MGMT expression and a possible role for MGMT in the ALT mechanism is discussed. Further analysis of the microarray data identified two groups of co-regulated genes (p < 5x10-5): CEBPA, TACC2, SFXN4, HNRPK and MGMT, and SIGIRR, LEF1, NSBP1 and SATB1. Two thirds of differentially expressed genes were down-regulated in ALT. Chromosomes 10 and 15 had a bias towards genes with lower expression in ALT while chromosomes 1, 4, 14 and X had a bias towards genes with higher expression levels in ALT. This work has developed a robust assay for ALT in tumour specimens which was then used to show the significance of ALT in sarcomas, astrocytomas and NSCLC. It has also identified genes that could possibly be molecular targets for the treatment of ALT[+] cancers.
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9

Henson, Jeremy D. "The role of Alternative Lengthening of Telomeres in human cancer." University of Sydney, 2006. http://hdl.handle.net/2123/1533.

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Doctor of Philosophy<br>Activation of a telomere maintenance mechanism is a vital step in the development of most cancers and provides a target for the selective killing of cancer cells. Cancers can use either telomerase or Alternative Lengthening of Telomeres (ALT) to maintain their telomeres and inhibition of either telomere maintenance mechanism can cause cancer cells to undergo senescence or apoptosis. Although telomerase inhibitors are undergoing clinical trials, on commencing this study very little was known about the role of ALT in cancer, what proteins were involved in its mechanism and regulation and how it could be targeted clinically. The primary aim of this thesis was to develop an assay for ALT suitable for examining archived tumour specimens and to begin using it to examine the prevalence and clinical significance of ALT in cancer. This assay and gene expression analysis was also used to identify genes that are involved in or associated with the activation of the ALT mechanism, to contribute towards the overall goal of an ALT cancer therapy. The ALT mechanism involves recombination mediated replication and ALT cells have a marked increase in a range of recombinational events specifically at their telomeres. Presumably, as a consequence of this the telomere lengths of ALT cells are very heterogeneous and on average long. This can be detected by terminal restriction fragment (TRF) Southern analysis, which has been used previously as the definitive test for ALT activity. However, TRF analysis requires intact genomic DNA and is unsuitable for tumour specimens which are commonly archived by paraffin embedding. Another hallmark of ALT is ALT-associated PML bodies (APBs) which are the subset of PML bodies that contain telomeric DNA. Work done in this study to consolidate APBs as a hallmark of ALT, combined with published data, showed 29/31 ALT[+], 3/31 telomerase[+] and 0/10 mortal cell lines/strains are APB[+]. The three APB[+]/telomerase[+] cell lines identified here had an order of magnitude lower frequency of APB[+] nuclei than the ALT[+] cell lines. APBs may be functionally linked to the ALT mechanism and contain the recombination proteins that are thought to be involved in the ALT mechanism. This study, in collaboration with Dr W-Q Jiang, strengthened this functional link by demonstrating that loss of ALT activity (as determined by TRF analysis) coincided with the disruption of APBs. The detection of APBs was developed into a robust assay for ALT in archived tumour specimens using a technique of combined immunofluorescence and telomere fluorescence in situ hybridisation. It was demonstrated that the APB assay concurred exactly with the standard assay for ALT (TRF analysis) in 60 tumours for which TRF analysis gave unequivocal results. The APB assay may be a more appropriate technique in the case of tumour specimen heterogeneity, which may explain why the APB assay was able to give definitive results when TRF analysis was equivocal. We demonstrated that intratumoral heterogeneity for ALT does exist and this could explain why about 3% of tumours in this study were APB[+] but with more than a ten-fold reduction in the frequency of APB[+] nuclei. This study also made the novel discovery of single stranded C-rich telomeric DNA inside APBs which potentially could be used to make the APB assay more suitable for routine pathology laboratory use. The APB assay was used to show that ALT is a significant concern for oncology. ALT was utilised in approximately one quarter of glioblastoma multiforme (GBM), one third of soft tissue sarcomas (STS) including three quarters of malignant fibrous histiocytomas (MFH), half of osteosarcomas and one tenth of non-small cell lung carcinomas (NSCLC). Furthermore, the patients with these ALT[+] tumours had poor survival; median survivals were 2 years for ALT[+] GBM, 4 years for ALT[+] STS including 3.5 years for ALT[+] MFH and 5 years for ALT[+] osteosarcoma. ALT[+] STS and osteosarcomas were also just as aggressive as their ALT[-] counterparts in terms of grade and patient outcome. ALT status was not found to be associated with response to chemotherapy in osteosarcomas or survival in STS. ALT was however, less prevalent in metastatic STS. The APB assay was a prognostic indicator for GBM and was correlated with three fold increased median survival in GBM (although this survival was still poor). ALT was more common in lower grade astrocytomas (88% ALT[+]) than GBM (24% ALT[+]) and ALT[+] GBM had an identical median age at diagnosis to that reported for secondary GBM. It is discussed that these data indicate that ALT was indirectly associated with secondary GBM and is possibly an early event in its progression from lower grade astrocytoma. This is relevant because secondary GBM have distinct genetic alterations that may facilitate activation of the ALT mechanism. Putative repressors of ALT could explain why this study found that ALT varied among the different STS subtypes. ALT was common in MFH (77%), leiomyosarcoma (62%) and liposarcoma (33%) but rare in rhabdomyosarcoma (6%) and synovial sarcoma (9%). ALT was not found in colorectal carcinoma (0/31) or thyroid papillary carcinoma (0/17) which have a high prevalence of telomerase activity and a reduced need for a telomere maintenance mechanism (low cell turnover), respectively. A yeast model of ALT predicts that one of the five human RecQ helicases may be required for ALT. Using the APB assay to test for the presence of ALT in tumours from patients with known mutations in either WRN or RECQL4 it was demonstrated that neither of these RecQ helicases is essential for ALT. Although p53 and mismatch repair (MMR) proteins have been suggested to be possible repressors of ALT, there was no apparent increase in the frequency of ALT in tumours from patients with a germline mutation in p53 codon 273 or in colorectal carcinomas that had microsatellite instability and thus MMR deficiency. Also contrary to being a repressor of ALT but consistent with its ability to interact with a protein involved in the ALT mechanism, the MMR protein MLH1, was demonstrated to be present in the APBs of an ALT[+] cell line. To further test for genes that may be involved in the ALT mechanism or associated with its activation, RNA microarray was used to compare the gene expression of 12 ALT[+] with 12 matched telomerase[+] cell lines; 240 genes were identified that were significantly differentially expressed (p<0.005) between the ALT[+] and telomerase[+] cell lines. Only DRG2 and SFNX4 were significantly differentially expressed after adjusting for the estimated false positive rate. Overall, DRG2, MGMT and SATB1 were identified as most likely to be relevant to the ALT[+] tumours and Western analysis indicated that DRG2 and MGMT levels were down-regulated after activation of ALT and up-regulated after activation of telomerase, whereas SATB1 protein levels appeared to be up-regulated after immortalisation but to a higher degree with activation of ALT compared to telomerase. Since lack of MGMT is known to be a determinant of temozolomide sensitivity in GBM, the possibility that ALT and the APB assay could be used to predict temozolomide sensitivity is discussed. The microarray data was consistent with MGMT expression being suppressed by EGF (p < 0.05), indicating that caution may be needed with combining EGFR inhibitors with temozolomide in ALT cancers. One ALT[+] cell line which did not express MGMT had TTAA sequence in its telomeres. This could possibly have resulted from mutations due to lack of MGMT expression and a possible role for MGMT in the ALT mechanism is discussed. Further analysis of the microarray data identified two groups of co-regulated genes (p < 5x10-5): CEBPA, TACC2, SFXN4, HNRPK and MGMT, and SIGIRR, LEF1, NSBP1 and SATB1. Two thirds of differentially expressed genes were down-regulated in ALT. Chromosomes 10 and 15 had a bias towards genes with lower expression in ALT while chromosomes 1, 4, 14 and X had a bias towards genes with higher expression levels in ALT. This work has developed a robust assay for ALT in tumour specimens which was then used to show the significance of ALT in sarcomas, astrocytomas and NSCLC. It has also identified genes that could possibly be molecular targets for the treatment of ALT[+] cancers.
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10

Dagg, Rebecca Ann. "The extensive proliferation of human cancer cells with ever-shorter telomeres." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17341.

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Cellular immortalisation is currently regarded as an essential step in malignant transformation and is consequently considered a hallmark of cancer. Acquisition of replicative immortality is achieved by activation of a telomere lengthening mechanism (TLM), either telomerase or the alternative lengthening of telomeres (ALT), to counter normal telomere attrition. However, a proportion of malignancies are reported to be TLM-negative. The lack of serial untreated malignant human tumour samples over time has made it impossible to examine telomere length over time and hence determine whether they are truly TLM-deficient, or whether this is the result of false-negative assays. Here we describe a subset (11%) of high-risk neuroblastomas (NB) that lack evidence of any significant TLM activity despite a 51% 5-year mortality rate. Two NB cell lines derived from such tumours proliferated for 500 population doublings (PDs) with ever-shorter telomeres (EST). The EST cells had exceptionally long and heterogeneous telomere lengths as measured by terminal restriction fragment analysis and telomere fluorescence in situ hybridisation. Both cell lines were telomerase negative during culturing and did not have elevated markers of ALT or associated gene mutations. The telomeres of these cells shortened by 80 and 55 bases/PD, consistent with telomere attrition due to normal cell division, but did not reach senescence after 500 PDs in culture. This is conclusive evidence that cells from highly malignant, lethal tumours are able to undergo continuous proliferation in spite of an EST phenotype. The EST phenotype was rescued by activation of telomerase (via transduction with hTERT expression constructs) or ALT (spontaneous occurrence of a nonsense TP53 mutation, followed by spontaneous activation of ALT after 100 PDs). We also found that NB EST cells are very sensitive to topoisomerase I inhibitors indicating the potential to target the EST phenotype with topoisomerase I inhibitors in high-risk NB.
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Książki na temat "Telomeres"

1

Double, John A., and Michael J. Thompson. Telomeres and Telomerase. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592591892.

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2

Songyang, Zhou, ed. Telomeres and Telomerase. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3.

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Songyang, Zhou, ed. Telomeres and Telomerase. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8.

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4

Foundation, Ciba, ed. Telomeres and telomerase. Chichester: John Wiley & Sons, 1997.

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5

Hiyama, Keiko, ed. Telomeres and Telomerase in Cancer. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-879-9.

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A, Double John, and Thompson Michael J, eds. Telomeres and telomerase: Methods and protocols. Totowa, N.J: Humana Press, 2002.

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7

Titia, De Lange, Lundblad Vicki, and Blackburn Elizabeth H, eds. Telomeres. 2nd ed. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2006.

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8

H, Blackburn Elizabeth, and Greider Carol W, eds. Telomeres. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1995.

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9

Tsatsakis, Aristidis. Telomeres. New York: Jenny Stanford Publishing, 2024. http://dx.doi.org/10.1201/9781003568094.

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10

Chadwick, Derek J., and Gail Cardew, eds. Ciba Foundation Symposium 211 - Telomeres and Telomerase. Chichester, UK: John Wiley & Sons, Ltd., 1997. http://dx.doi.org/10.1002/9780470515433.

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Części książek na temat "Telomeres"

1

Joseph, Nithila A., Chi-Fan Chen, Jiun-Hong Chen, and Liuh-Yow Chen. "Monitoring Telomere Maintenance During Regeneration of Annelids." In Methods in Molecular Biology, 467–78. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2172-1_24.

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AbstractTelomere shortening is a hallmark of aging and eventually constrains the proliferative capacity of cells. The protocols discussed here are used for monitoring telomeres comprehensively in Aeolosoma viride, a model system for regeneration studies. We present methods for analyzing the activity of telomerase enzyme in regenerating tissue by telomeric repeat amplification protocol (TRAP) assay, for comparing telomere length between existing tissue and newly regenerated tissue by telomere restriction fragment (TRF) assay, as well as for visualizing telomeres by fluorescence in situ hybridization (FISH).
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2

Gomes, N. M. V., J. W. Shay, and W. E. Wright. "Telomeres and Telomerase." In The Comparative Biology of Aging, 227–58. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3465-6_11.

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3

Songyang, Zhou. "Introduction to Telomeres and Telomerase." In Telomeres and Telomerase, 1–11. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_1.

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4

Xin, Huawei. "Telomeric Repeat Amplification Protocol: Measuring the Activity of the Telomerase." In Telomeres and Telomerase, 107–11. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_10.

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5

Williams, Eli S., Michael N. Cornforth, Edwin H. Goodwin, and Susan M. Bailey. "CO-FISH, COD-FISH, ReD-FISH, SKY-FISH." In Telomeres and Telomerase, 113–24. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_11.

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Abreu, Eladio, Rebecca M. Terns, and Michael P. Terns. "Visualization of Human Telomerase Localization by Fluorescence Microscopy Techniques." In Telomeres and Telomerase, 125–37. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_12.

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Multani, Asha S., and Sandy Chang. "Cytogenetic Analysis of Telomere Dysfunction." In Telomeres and Telomerase, 139–43. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_13.

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Rai, Rekha, and Sandy Chang. "Probing the Telomere Damage Response." In Telomeres and Telomerase, 145–50. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_14.

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Ma, Wenbin. "Analysis of Telomere Proteins by Chromatin Immunoprecipitation (ChIP)." In Telomeres and Telomerase, 151–59. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_15.

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Ma, Wenbin, Hyeung Kim, and Zhou Songyang. "Studying of Telomeric Protein–Protein Interactions by Bi-Molecular Fluorescence Complementation (BiFC) and Peptide Array-Based Assays." In Telomeres and Telomerase, 161–71. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_16.

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Streszczenia konferencji na temat "Telomeres"

1

Yin, J., Z. Zhang, and Z. Song. "Terahertz waves enhance telomerase activity and prolong cellular telomere length." In 2024 IEEE International Conference on Plasma Science (ICOPS), 1. IEEE, 2024. http://dx.doi.org/10.1109/icops58192.2024.10625849.

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Soboleva, O. A., A. V. Torgunakova, and V. I. Minina. "TELOMERE LENGTH IN PATIENTS WITH LUNG CANCER." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-373.

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An analysis was made of the relative length of telomeres and rs2736100 polymorphic variants of the TERT gene in 123 patients diagnosed with lung cancer and 120 healthy individuals. The telomeres of cancer patients turned out to be statistically significantly longer (p&lt;0,001) compared to healthy ones. Depending on the carriage of various variants of the TERT genotypes, there were no significant differences in telomere length in both groups.
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3

Sannikova, A. V., M. R. Sharipova, E. V. Shakirov, and L. R. Valeeva. "THE ROLE OF TRFL PROTEINS IN THE REGULATION OF TELOMERE LENGTH MARCHANTIA POLYMORPHA." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-368.

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Telomeres are nucleoprotein structures, involved in protection of the physical ends of eukaryotic chromosomes. A decisive role in maintaining telomere stability is played by specific proteins telomere complex are TRF proteins. Here, we have shown the intraspecific variability of telomere length and the involvement of TRFL protein in telolere length maintanance in a liverwort M. polymorpha as a new model plant for telomere biology studies.
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4

Shay, Jerry. "Abstract ED04-01: Aging and cancer: are telomeres and telomerase the connection?" In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-ed04-01.

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Lin, Clement, Guanhui Wu, Kaibo Wang, Buket Onel, Saburo Sakai, and Danzhou Yang. "Abstract 1856: Targeting human telomeres by binding of epiberberine to telomeric G-quadruplex." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1856.

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Lin, Clement, Guanhui Wu, Kaibo Wang, Buket Onel, Saburo Sakai, and Danzhou Yang. "Abstract 1856: Targeting human telomeres by binding of epiberberine to telomeric G-quadruplex." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1856.

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Huang, Chenhui, Xueyu Dai, and Weihang Chai. "Abstract 2039: Human Stn1 protects telomere integrity by promoting efficient lagging strand synthesis at telomeres." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2039.

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Poon, S. S. S., R. W. Ward, and P. M. Lansdorp. "Segmenting telomeres and chromosomes in cells." In 1999 IEEE International Conference on Acoustics, Speech, and Signal Processing. Proceedings. ICASSP99 (Cat. No.99CH36258). IEEE, 1999. http://dx.doi.org/10.1109/icassp.1999.757575.

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Cao, En-Hua, Ai Chen, Xueguang Sun, Xiaoyan Zhang, Jingfen Qin, Dage Liu, Chen Wang, and Chunli Bai. "Formation of sequence-specific telomeric DNA loops via direct effects of psoralen-photosensitization on telomeres." In Optics and Optoelectronic Inspection and Control: Techniques, Applications, and Instruments, edited by Hong Liu and Qingming Luo. SPIE, 2000. http://dx.doi.org/10.1117/12.403922.

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Bechter, Oliver E., and Margit Dlaska. "Abstract 2993: Homologous recombination between telomeres is present in ALT and telomerase-positive immortal cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2993.

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Raporty organizacyjne na temat "Telomeres"

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Paul, Satashree. How Early Life Stress Effects Telomeres in Later Life. Spring Library, April 2021. http://dx.doi.org/10.47496/nl.blog.25.

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Wahl, G. M. [An homologous recombination strategy to directly clone mammalian telomeres]. Progress report. Office of Scientific and Technical Information (OSTI), July 1994. http://dx.doi.org/10.2172/10163039.

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Lundblad, Victoria. Telomere Maintenance in the Absence of Telomerase. Fort Belvoir, VA: Defense Technical Information Center, April 2000. http://dx.doi.org/10.21236/ada392106.

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Zwang, Yaara. Systematic Characterization of the Molecular Mechanisms That Regulate and Mediate Alternative Lengthening of Telomeres in Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada607152.

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Zwang, Yaara. Systematic Characterization of the Molecular Mechanisms That Regulate and Mediate Alternative Lengthening of Telomeres in Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada581164.

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Wahl, G. M. An homologous recombination strategy to directly clone mammalian telomeres. Final progress report, March 15, 1991--March 14, 1994. Office of Scientific and Technical Information (OSTI), June 1994. http://dx.doi.org/10.2172/10196406.

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Fordyca, Colleen, and Jeffrey Griffith. Telomere DNA Content, Telomerase, and c-Myc Amplification in Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396805.

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Broccoli, Dominique. Telomerase Independent Telomere Maintenance in Ovarian Cancer: A Molecular Genetic Analysis. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407268.

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Broccoli, Dominique. Telomerase Independent Telomere Maintenance in Ovarian Cancer: A Molecular Genetic Analysis. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada428241.

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Pennock, Erin, and Vicki Lundblad. Identification of New Genes that Regulate Telomerase and Telomere Length in Budding Yeast. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395954.

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