Relevant bibliographies by topics / Telomeres maintenance mechanism

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Academic literature on the topic 'Telomeres maintenance mechanism'

Author: Grafiati
Published: 7 September 2022
Last updated: 18 September 2022

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Journal articles on the topic "Telomeres maintenance mechanism"

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Lin, Chi-Ying, Hsih-Hsuan Chang, Kou-Juey Wu, Shun-Fu Tseng, Chuan-Chuan Lin, Chao-Po Lin, and Shu-Chun Teng. "Extrachromosomal Telomeric Circles Contribute to Rad52-, Rad50-, and Polymerase δ-Mediated Telomere-Telomere Recombination in Saccharomyces cerevisiae." Eukaryotic Cell 4, no. 2 (February 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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Royle, Nicola J., Aarón Méndez-Bermúdez, Athanasia Gravani, Clara Novo, Jenny Foxon, Jonathan Williams, Victoria Cotton, and Alberto Hidalgo. "The role of recombination in telomere length maintenance." Biochemical Society Transactions 37, no. 3 (May 20, 2009): 589–95. http://dx.doi.org/10.1042/bst0370589.

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Human telomeres shorten during each cell division, predominantly because of incomplete DNA replication. This eventually results in short uncapped telomeres that elicit a DNA-damage response, leading to cellular senescence. However, evasion of senescence results in continued cell division and telomere erosion ultimately results in genome instability. In the long term, this genome instability is not sustainable, and cancer cells activate a TMM (telomere maintenance mechanism), either expression of telomerase or activation of the ALT (alternative lengthening of telomeres) pathway. Activation of the ALT mechanism results in deregulation of recombination-based activities at telomeres. Thus ALT+ cells show elevated T-SCE (telomere sister-chromatid exchange), misprocessing of t-loops that cap chromosomes and recombination-based processes between telomeres or between telomeres and ECTRs (extrachromosomal telomeric repeats). Some or all of these processes underlie the chaotic telomere length maintenance that allows cells in ALT+ tumours unlimited replicative capacity. ALT activation is also associated with destabilization of a minisatellite, MS32. The connection between the minisatellite instability and the deregulation of recombination-based activity at telomeres is not understood, but analysis of the minisatellite can be used as a marker for ALT. It is known that telomere length maintenance in ALT+ cells is dependent on the MRN [MRE11 (meiotic recombination 11)–Rad50–NBS1 (Nijmegen breakage syndrome 1)] complex, but knowledge of the role of other genes, including the Werner's (WRN) and Bloom's (BLM) syndrome DNA helicase genes, is still limited.
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Chen, W., S. M. Chen, Y. Yu, B. K. Xiao, Z. W. Huang, and Z. Z. Tao. "Telomerase inhibition alters telomere maintenance mechanisms in laryngeal squamous carcinoma cells." Journal of Laryngology & Otology 124, no. 7 (April 20, 2010): 778–83. http://dx.doi.org/10.1017/s0022215109992854.

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AbstractBackground and purpose:Telomere length must be maintained throughout cancer cell progression and proliferation. In most tumours, telomerase activity maintains telomere length. Therefore, telomerase is a target for cancer treatments. However, some cancer cells maintain telomere length through an alternative mechanism termed ‘alternative lengthening of telomeres’. To determine how telomerase inhibition relates to the initiation of the alternative lengthening of telomeres pathway, we investigated telomerase activity and telomere maintenance in Hep-2 cells with and without reduced telomerase activity.Materials and methods:We investigated telomerase activity levels in a normal Hep-2 cell line and in residual cells following telomerase inhibition treatment. Additionally, we looked for expression of a marker protein for the alternative lengthening of telomeres mechanism.Results and conclusions:In the residual cells, telomerase activity was eliminated. However, these cells had higher levels of the alternative lengthening of telomeres biomarker, suggesting an alternative mechanism for telomere maintenance following telomerase inhibition. These results could have a major impact on the design of new cancer treatments.
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Niida, Hiroyuki, Yoichi Shinkai, M. Prakash Hande, Takehisa Matsumoto, Shoko Takehara, Makoto Tachibana, Mitsuo Oshimura, Peter M. Lansdorp, and Yasuhiro Furuichi. "Telomere Maintenance in Telomerase-Deficient Mouse Embryonic Stem Cells: Characterization of an Amplified Telomeric DNA." Molecular and Cellular Biology 20, no. 11 (June 1, 2000): 4115–27. http://dx.doi.org/10.1128/mcb.20.11.4115-4127.2000.

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ABSTRACT Telomere dynamics, chromosomal instability, and cellular viability were studied in serial passages of mouse embryonic stem (ES) cells in which the telomerase RNA (mTER) gene was deleted. These cells lack detectable telomerase activity, and their growth rate was reduced after more than 300 divisions and almost zero after 450 cell divisions. After this growth crisis, survivor cells with a rapid growth rate did emerge. Such survivors were found to maintain functional telomeres in a telomerase-independent fashion. Although telomerase-independent telomere maintenance has been reported for some immortalized mammalian cells, its molecular mechanism has not been elucidated. Characterization of the telomeric structures in one of the survivor mTER −/− cell lines showed amplification of the same tandem arrays of telomeric and nontelomeric sequences at most of the chromosome ends. This evidence implicatescis/trans amplification as one mechanism for the telomerase-independent maintenance of telomeres in mammalian cells.
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Calado, Rodrigo T., Solomon A. Graf, and Neal S. Young. "Telomeric Recombination in Lymphocytes Implicates ALT, an Alternative Mechanism for Telomere Length Maintenance, in Normal Human Hematopoietic Cells." Blood 110, no. 11 (November 16, 2007): 1332. http://dx.doi.org/10.1182/blood.v110.11.1332.1332.

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Abstract Telomeres are the very ends of chromosomes and protect the genome from recombination, end-to-end-fusion, and recognition as damaged DNA. Telomeres are eroded with each cell division, eventually reaching such critically short length as to cause cell cycle arrest, apoptosis, or genomic instability. In most highly proliferative cells, including hematopoietic stem cells and T lymphocytes, telomere attrition is countered by telomere extension by telomerase reverse transcriptase complex. The majority of cancer cells also express telomerase, which maintains telomere length and allows indefinite cell proliferation. However, about 10% of tumors maintain telomere length in the absence of telomerase by mechanisms collectively termed alternative lengthening of telomeres (ALT). ALT mainly acts through asymmetrical exchange of telomeric material between chromosomes or sister chromatids, producing one daughter-cell with short telomeres and a limited life-span and its sister with long telomeres and higher proliferative capacity. To date, ALT has only been reported in cancer cells or through genetic engineering of mammalian cells. Here we investigated whether ALT mechanisms were active in hematopoietic cells using chromosome orientation fluorescent in situ hybridization (CO-FISH). In standard FISH, a telomeric probe produces fours signals per chromosome, one at each end of the two chromatids. Using CO-FISH, the newly synthesized DNA strand is fragmented by BrdU incorporation and UV light exposure and then digested by exonucleases. In CO-FISH, a telomeric probe produces two signals only, one at each end of the chromosome; in the presence of telomeric recombination, the telomeric signal is split, generating more than two signals per chromosome. Peripheral blood lymphocytes from three healthy volunteers, normal human fibroblasts, K562 cells, telomerase-positive HeLa cells (known to be negative for ALT),and telomerase-negative VA13 cells (known to be positive for ALT) were investigated for telomeric sister chromatid exchange (t-SCE); at least 20 metaphases per cell type were examined. Cultured peripheral blood lymphocytes and VA13 cells both showed increased levels of telomeric sister chromatid exchange in comparison to the other cells (P=0.0001): telomeric probe generated 2.62±0.11 telomeric signals/chromosome in lymphocytes; 2.23±0.04 in VA13 cells; 2.09±0.01 in HeLa cells; 2.02±0.01 in K562 cells; and 2.02±0.01 in human skin fibroblasts. Staining incorporated-BrdU over 24 hours and evaluation of “harlequin” chromosomes point to a similar rate of genomic sister chromatid exchange in lymphocytes, VA13 cells, and HeLa cells, suggesting that high chromatid exchange is confined to the telomeric region. A physical association between promyelocytic leukemia protein (PML) and telomeres is characteristic of some ALT-positive cells, but confocal microscopy failed to co-localize the telomeric probe and anti-PML monoclonal antibody in peripheral blood lymphocytes, suggesting that t-SCE in lymphocytes is not mediated by PML. This is the first demonstration of ALT activation in normal mammalian cells. ALT may be activated in peripheral blood lymphocytes as a complementary mechanism to maintain telomere length, and may explain the differences in age-related telomere shortening observed between lymphocytes and granulocytes.
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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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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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Amato, Roberta, Martina Valenzuela, Francesco Berardinelli, Erica Salvati, Carmen Maresca, Stefano Leone, Antonio Antoccia, and Antonella Sgura. "G-quadruplex Stabilization Fuels the ALT Pathway in ALT-positive Osteosarcoma Cells." Genes 11, no. 3 (March 13, 2020): 304. http://dx.doi.org/10.3390/genes11030304.

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Most human tumors maintain telomere lengths by telomerase, whereas a portion of them (10–15%) uses a mechanism named alternative lengthening of telomeres (ALT). The telomeric G-quadruplex (G4) ligand RHPS4 is known for its potent antiproliferative effect, as shown in telomerase-positive cancer models. Moreover, RHPS4 is also able to reduce cell proliferation in ALT cells, although the influence of G4 stabilization on the ALT mechanism has so far been poorly investigated. Here we show that sensitivity to RHPS4 is comparable in ALT-positive (U2OS; SAOS-2) and telomerase-positive (HOS) osteosarcoma cell lines, unlinking the telomere maintenance mechanism and RHPS4 responsiveness. To investigate the impact of G4 stabilization on ALT, the cardinal ALT hallmarks were analyzed. A significant induction of telomeric doublets, telomeric clusterized DNA damage, ALT-associated Promyelocytic Leukaemia-bodies (APBs), telomere sister chromatid exchanges (T-SCE) and c-circles was found exclusively in RHPS4-treated ALT cells. We surmise that RHPS4 affects ALT mechanisms through the induction of replicative stress that in turn is converted in DNA damage at telomeres, fueling recombination. In conclusion, our work indicates that RHPS4-induced telomeric DNA damage promotes overactivation of telomeric recombination in ALT cells, opening new questions on the therapeutic employment of G4 ligands in the treatment of ALT positive tumors.
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Marchesini, M., R. Matocci, L. Tasselli, V. Cambiaghi, A. Orleth, L. Furia, C. Marinelli, et al. "PML is required for telomere stability in non-neoplastic human cells." Oncogene 35, no. 14 (June 29, 2015): 1811–21. http://dx.doi.org/10.1038/onc.2015.246.

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Abstract Telomeres interact with numerous proteins, including components of the shelterin complex, whose alteration, similarly to proliferation-induced telomere shortening, initiates cellular senescence. In tumors, telomere length is maintained by Telomerase activity or by the Alternative Lengthening of Telomeres mechanism, whose hallmark is the telomeric localization of the promyelocytic leukemia (PML) protein. Whether PML contributes to telomeres maintenance in normal cells is unknown. We show that in normal human fibroblasts the PML protein associates with few telomeres, preferentially when they are damaged. Proliferation-induced telomere attrition or their damage due to alteration of the shelterin complex enhances the telomeric localization of PML, which is increased in human T-lymphocytes derived from patients genetically deficient in telomerase. In normal fibroblasts, PML depletion induces telomere damage, nuclear and chromosomal abnormalities, and senescence. Expression of the leukemia protein PML/RARα in hematopoietic progenitors displaces PML from telomeres and induces telomere shortening in the bone marrow of pre-leukemic mice. Our work provides a novel view of the physiologic function of PML, which participates in telomeres surveillance in normal cells. Our data further imply that a diminished PML function may contribute to cell senescence, genomic instability, and tumorigenesis.
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Idilli, Aurora Irene, Francesca Pagani, Emanuela Kerschbamer, Francesco Berardinelli, Manuel Bernabé, María Luisa Cayuela, Silvano Piazza, Pietro Luigi Poliani, Emilio Cusanelli, and Maria Caterina Mione. "Changes in the Expression of Pre-Replicative Complex Genes in hTERT and ALT Pediatric Brain Tumors." Cancers 12, no. 4 (April 22, 2020): 1028. http://dx.doi.org/10.3390/cancers12041028.

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Background: The up-regulation of a telomere maintenance mechanism (TMM) is a common feature of cancer cells and a hallmark of cancer. Routine methods for detecting TMMs in tumor samples are still missing, whereas telomerase targeting treatments are becoming available. In paediatric cancers, alternative lengthening of telomeres (ALT) is found in a subset of sarcomas and malignant brain tumors. ALT is a non-canonical mechanism of telomere maintenance developed by cancer cells with no-functional telomerase. Methods: To identify drivers and/or markers of ALT, we performed a differential gene expression analysis between two zebrafish models of juvenile brain tumors, that differ only for the telomere maintenance mechanism adopted by tumor cells: one is ALT while the other is telomerase-dependent. Results: Comparative analysis of gene expression identified five genes of the pre-replicative complex, ORC4, ORC6, MCM2, CDC45 and RPA3 as upregulated in ALT. We searched for a correlation between telomerase levels and expression of the pre-replicative complex genes in a cohort of paediatric brain cancers and identified a counter-correlation between telomerase expression and the genes of the pre-replicative complex. Moreover, the analysis of ALT markers in a group of 20 patients confirmed the association between ALT and increased RPA and decreased H3K9me3 localization at telomeres. Conclusions: Our study suggests that telomere maintenance mechanisms may act as a driver of telomeric DNA replication and chromatin status in brain cancers and identifies markers of ALT that could be exploited for precise prognostic and therapeutic purposes.
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Dissertations / Theses on the topic "Telomeres maintenance mechanism"

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Billard, Pauline. "Maintenance télomérique : intérêt dans le diagnostic des gliomes en lien avec le métabolisme mitochondrial." Thesis, Lyon, 2021. http://www.theses.fr/2021LYSE1303.

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Le complexe Shelterin, composé de 6 protéines (POT1 / TRF1 / TRF2 / TIN2 / RAP1 et ACD) joue un rôle majeur au niveau des télomères. Ainsi, il permet la protection de l’extrémité simple brin par la formation de la D-loop, la régulation de la signalisation des voies de dommages à l’ADN ; il participe à la réplication des télomères et contrôle l’accessibilité et la processivité de la télomérase, unique enzyme permettant l’allongement des télomères. Au cours de cette thèse, mon travail s’est organisé autour de 2 principaux axes, le premier, fondamental s’est intéressé aux effets extra-télomériques de la protéine ACD (anciennement appelée TPP1). Le deuxième, plus transversal s’est attardé sur les processus de maintenance des télomères dans le cas des gliomes. Concernant le premier aspect, il est maintenant connu que la protéine ACD fait le lien entre TIN2 et TERT (sous unité catalytique de la télomérase) aux télomères. Ces deux protéines peuvent aussi partiellement se localiser à la mitochondrie et y possèdent alors divers effets sur le métabolisme, la régulation du stress oxydant ou encore la mitophagie. Ainsi, et suite à des prédictions in silico de potentiel MTS pour ACD, nous avons émis l’hypothèse qu’ACD pourrait être le partenaire manquant de TIN2 et TERT à la mitochondrie. Dans ce cas il restait alors à identifier ses fonctions mitochondriales. Après avoir démontré la localisation partielle d’ACD à la mitochondrie par différentes méthodes, nous avons pu mettre en évidence son influence dans la protection contre le stress oxydatif. Ainsi la surexpression d’ACD réduit la production secondaire de radicaux oxygénés mitochondriaux et la perte d’ADN mitochondrial. Le stress oxydatif causant la réduction des foci mitochondriaux d’ACD. Dans un second temps, nous nous sommes intéressés aux mécanismes de maintenance des télomères (TMM) que les cellules cancéreuses acquièrent afin d’outrepasser la sénescence réplicative. Dans ce sens, les tumeurs peuvent réactiver la télomérase (95% des cas) ou utiliser un processus alternatif (ALT) basé sur la recombinaison homologue (5% des cas). Pour les gliomes, jusqu’à 25% des tumeurs utilisent le processus ALT, associé à la perte d’ATRX, les autres gliomes utilisent la télomérase et présentent classiquement une mutation du promoteur de TERT (TERTmt). Ces deux marqueurs moléculaires ont par ailleurs une valeur diagnostique et pronostique et font parties des critères de classification histo-moléculaire de l’OMS . Or, de 4 à 28% des gliomes (selon les sous-types) ne possèdent ni altération d’ATRX ni mutation de TERT suggérant une activation de l’un des TMM par d’autres altérations voire d’autres voies. Dans ce sens, nous avons développé un test mesurant le TMM vrai en nous basant sur la recherche des c-circle (un marqueur du ALT) et proposé un algorithme breveté (TeloDiag) prenant en compte ce TMM, les mutations d’IDH et le grading histologique. Le TeloDiag permet de re-classer 38% des gliomes atypiques (au niveau moléculaire). Il a généré une nouvelle catégorie de tumeurs de haut grade IDHwt et ALT+, n’existant pas dans la classification OMS et montrant une tendance à un meilleur pronostic que les glioblastomes IDHwt (TERTmt). Enfin, nous avons apporté la preuve de concept de la faisabilité de ce test en circulant, pour les astrocytomes IDHmt
The Shelterin complex, made of 6 proteins (POT1 / TRF1 / TRF2 / TIN2 / RAP1 and ACD) plays a major role in telomeres. Thus, it allows the protection of the telomeric single-stranded end by the formation of the D-loop, the regulation of DNA damage signaling pathways; it participates in telomere replication and controls the accessibility and processivity of the telomerase, the unique enzyme allowing telomere lengthening. During this thesis, my work was organized in 2 main axes, the first, fundamental, was interested in the extra-telomeric effects of the ACD protein (also called TPP1). The second, more transversal, focused on the processes of telomere maintenance in gliomas. Concerning the first aspect, it is now known that the ACD protein makes the link between TIN2 and TERT (catalytic subunit of telomerase) in the telomeres. These two proteins can also partially localize to the mitochondria and then have various effects on mitochondrial metabolism, on the oxidative stress regulation or on the mitophagy process. Thus, and following in silico predictions of a putative MTS for ACD, we hypothesized that ACD could be the missing partner of TIN2 and TERT in the mitochondria. In this case, it then remained to identify its mitochondrial functions. After demonstrating the partial localization of ACD in the mitochondria by different methods, we were able to demonstrate its influence in the protection against oxidative stress. Thus overexpression of ACD reduces secondary production of mitochondrial oxygen radicals and loss of mitochondrial DNA. Oxidative stress causing reduction of ACD mitochondrial foci. Secondly, we looked at the telomere maintenance mechanisms (TMM) that cancer cells acquire in order to override replicative senescence. In this sense, tumors can reactivate telomerase (95% of cancer) or use an alternative process (ALT) based on homologous recombination (5% of cancer). In the case of gliomas, up to 25% of tumors use the ALT process, associated with the loss of ATRX, the other gliomas use telomerase and typically have a mutation of the TERT promoter (TERTmt). These two molecular markers also have diagnostic and prognostic value and are part of the WHO histo-molecular classification criteria. But, 4 to 28% of gliomas (depending on the subtypes) do not have an ATRX alteration or TERT mutation suggesting activation of one of the TMM by other alterations or even other pathways. In this sense, we have developed a test measuring the true TMM based on the detection of c-circles (a marker of ALT) and proposed a patented algorithm (TeloDiag) taking into account this TMM, IDH mutations and the histological grading. The TeloDiag makes it possible to re-classify 38% of atypical gliomas (at the molecular level). It generated a new category of high grade IDHwt and ALT + tumors, not found in the WHO classification and showing a tendency for a better prognosis than IDHwt glioblastomas (TERTmt). Finally, we provided the proof of concept of the feasibility of this circulating test for IDHmt astrocytomas
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Bakhos, Al Douaihy Dalal. "Implication des lysines acétyl transférases dans les mécanismes ALTernatifs de maintenance des télomères Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance ALT cancer cells are specifically sensitive to lysine acetyl transferase inhibition." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2322&f=12888.

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Certaines cellules cancéreuses peuvent utiliser un mécanisme indépendant de la télomérase, connu sous le nom ALT (Alternative Lengthening of Telomeres) pour allonger leurs télomères. Les cellules ALT sont caractérisées par des télomères hétérogènes extrêmement longs et d’autres très courts voire indétectables qui co-localisent avec les corps PML pour former des structures nucléaires appelées APB (ALT-associated PML Bodies), et une fréquence élevée d'échange entre les télomères des chromatides sœurs appelées T- SCE (Telomeric Sister Chromatid Exchange). Bien qu'il soit concevable que la recombinaison homologue soit le mécanisme clé pour le maintien des télomères par la voie ALT, les acteurs moléculaires ne sont pas très bien connus. Nous avons identifié de nouveaux régulateurs potentiellement impliqués dans le mécanisme ALT: PCAF (P300/CBP-associated factor) et GCN5 (General Control Non-derepressible 5), deux lysines acétyl transférases homologues. Elles représentent généralement des facteurs de transcription, cependant, elles peuvent aussi acétyler des protéines non histones. Elles sont mutuellement exclusives dans de multiples complexes y compris le complexe SAGA. Nous avons montré que l’inhibition de ces deux protéines induit des effets opposés sur le phénotype ALT. Bien que l’absence de GCN5 augmentait l'instabilité des télomères et la fréquence des T-SCE et, la sous-expression de PCAF diminuait les T-SCE, la formation des APB et l'instabilité des télomères. Nos résultats suggèrent que dans les cellules ALT GCN5 est présent au niveau de l’ADN télomérique il inhibe la recombinaison entre les télomères et n’affecte pas la formation des APB, contrairement à PCAF qui peut indirectement les favoriser et stimuler aussi la formation des APB. Ensuite, nous avons cherché les mécanismes par lesquels PCAF et GCN5 contribuent au maintien des télomères dans les cellules ALT. Nous avons proposé que la participation de ces deux protéines consiste à réguler le turnover de la protéine télomérique TRF1 via USP22, une déubiquitinase identifiée pour la première fois comme un constituant des APB. En outre, l'intérêt de cibler l’activité de ces lysines acétyl transférase dans les cellules ALT a été testé in vitro en utilisant des inhibiteurs seuls ou combinés à l’irradiation. Nous avons montré que les cellules ALT sont particulièrement sensibles à l'inhibition de l'activité lysine acétyl transférase par l'acide anacardique (AA). Le traitement par cette molécule récapitule l'effet de la sous-expression de PCAF sur le phénotype ALT, suggérant que l’AA défavorise le mécanisme ALT en inhibant l'activité lysine acétyl transférase de PCAF, et non pas celle du GCN5. De plus, l'AA sensibilise spécifiquement les cellules ALT humaines à l’irradiation en comparant aux cellules télomérase-positives, prouvant que l'inhibition de l'activité des lysines acétyl transférases peut être un outil pour traiter les cellules ALT en augmentant l'efficacité de la radiothérapie
Some cancer cells can use a telomerase-independent mechanism, known as alternative lengthening of telomeres (ALT), to elongate their telomeres. ALT cells present unusual characteristics: extremely long and heterogeneous telomeres that colocalize with PML bodies to form nuclear structures called ALT-associated PML Bodies (APB), and high frequency of exchange events between sisters chromatid telomere referred to as Telomeric Sister Chromatid Exchange (T-SCE). Although it is agreed that homologous recombination is the key mechanism allowing the maintenance of the telomeres of ALT cells, the molecular actors involved are not yet known. We identified new actors potentially involved in the ALT mechanism: general control non-derepressible 5 (GCN5) and P300/CBP-associated factor (PCAF). Although they represent transcription factors, they can also acetylate non-histone proteins. They are mutually exclusive subunits in SAGA-like complexes. Here, we reveal that down regulation of GCN5 and PCAF had differential effects on some phenotypic characteristics of ALT cells. While GCN5 knockdown increased T-SCE and telomere instability, PCAF knockdown decreased T-SCE, APBs formation and telomere instability. GCN5 and PCAF knockdowns had thus differential effects on ALT, up-regulating it or down-regulating it respectively. Our results suggest that in ALT cells GCN5 is present at telomeres and opposes telomere recombination and does not affect the formation of APBs, unlike PCAF which may indirectly favour them and stimulate the APB formation. Then we evaluate the mechanisms by which PCAF and GCN5 contribute to the maintenance of telomeres in ALT cells. We have proposed that the participation of these two proteins should involve regulating the turnover of the telomeric protein TRF1 via USP22, a deubiquitinase identified for the first time as a component of APBs. In addition, the interest of targeting lysine acetyl transferase activities in ALT cells to oppose the maintenance of telomeres was subsequently tested in vitro using inhibitors alone or combined to irradiation. We have shown that ALT cells are particularly sensitive to the inhibition of acetyltransferases activities using Anacardic Acid (AA). AA treatment recapitulates the effect of PCAF knockdown on several ALT features, suggesting that AA decreased the ALT mechanism through the inhibition of lysine transferase activity of PCAF, but not that of GCN5. Furthermore, AA specifically sensitizes human ALT cells to radiation as compared to telomerase-positive cells suggesting that the inhibition of lysine acetyltransferases activity may be used to increase the radiotherapy efficiency against ALT cancers
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3

Gocha, April Renee Sandy. "Mechanisms of alternative telomere elongation in human cancer cells." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1351190051.

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4

Karpov, Victor. "A study on telomere protection and telomerase-and-cap-independent mechanisms of telomere maintenance in yeast Saccharomyces cerevisiae." Mémoire, Université de Sherbrooke, 2008. http://savoirs.usherbrooke.ca/handle/11143/3940.

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An SGA approach to discover cdc13-1ts supressors. Telomeres, the DNA-protein complexes at the end of eukaryotic chromosomes, are essential for chromosomal stability. In yeast, the telomeric single-strand binding protein Cdc13p has multiple important roles related to telomere maintenance: (1) telomeric"capping"--protection of telomeres by forming complexes with yKu70/80 and with Stn1p/Ten1p; (2) positive regulation of telomere replication via interaction with Est1p, which is a part of telomerase; (3) negative regulation of telomerase by the recruitment of telomere elongation suppressors Stn1p and Ten1p. In an attempt to identify genes that are involved in the deleterious outcome of an absence of Cdc13p, we screened the yeast gene knock-out library for genes that could suppress the growth defect of cdc13-1 cells at 33ê C. For this purpose, we performed an SGA array experiment. We scored for the ability of double mutant haploids to grow at 33ê C. Eventually, we hoped to find the elusive genes involved in telomere 5'-end processing (exonucleases). Based on the comparative analysis of growth properties of the strains (23ê C vs 33ê C), the initial screen identified up to 111 genes that displayed an apparent growth at 33ê C. In order to verify these results, diploids were regenerated, sporulated, microdissected, and haploid double mutants cdc13-1 yfg[deletion] were isolated from 38 potential cdc13-1 suppressors. Unfortunately, this verification failed to reproduce a suppression of the growth defect by any of the selected genes at any temperature. While disappointing, the results reemphasize that careful re-examination of large scale SGA approaches are indispensable before going on to more involved experimentation. Similarities and differences between adaptation to DNA double-strand break and to telomere uncapping in yeast Saccharomyces cerevisiae. It was previously shown that a certain proportion of telomerase negative survivor cells (both type I and type II cells) is able to survive in the absence of the telomere capping protein Cdc13p. These strains (named [deletion]13s) were characterized in great detail and one of their discovered features was a striking ability to continuously inactivate DNA-damage checkpoints. Based on structural similarities between DNA double strand breaks (DSB) and unprotected telomeres, we attempted to verify if the molecular mechanisms regulating adaptation to a single irreparable DSB also regulate adaptation to a loss of Cdc13p. For this purpose we created three tlc1[deletion] cdc13[deletion] strains also harboring DSB adaptation related mutations tid1[deletion], ptc2[deletion] and rfa1-t11. After deprotection of their telomeres, mutant survivor cells showed similar cell cycle progression patterns as compared to the cells where a single irreparable DSB was introduced. Adaptation defective mutants tid1[deletion] and ptc2[deletion] demonstrated an inability to adapt to telomere uncapping and to resume cell cycle. Interestingly, cells harboring the rfa1-t11 allele, which was reported to suppress adaptation defects of other mutations, did not show any distinguishable phenotype in terms of initial adaptation to telomere deprotection; i.e. rfa1-t11 mutant survivors do escape the G2/M arrest and re-enter the cell cycle. However, all three mutant survivor strains failed to produce viable [deletion]13 capping independent cells, which is consistent with the hypothesis that adaptation to loss of Cdc13p depends on the same pathway as the previously reported adaptation phenomenon. Finally, we report the surprising finding that if cells had once experienced an adapted [deletion]13 state, they will re-produce capping negative survivors much more readily. Thus, while a culture of type II survivor cells generates [deletion]13s at a rate of about 1×10 -5 events per division, cells that had been [deletion]13s and re-transformed with a Cdc13p carrying plasmid will produce capping independent cells at about 1×10-2 events per division. We are currently examining why these cells re-generate [deletion]13 cell lines more readily and suspect structural differences in telomere terminal sequence arrangements.
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Cabuy, Erik. "Investigations of telomere maintenance in DNA damage response defective cells and telomerase in brain tumours." Thesis, Brunel University, 2005. http://bura.brunel.ac.uk/handle/2438/5157.

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Telomeres are nucleoprotein complexes located at the end of chromosomes. They have an essential role in protecting chromosome ends. Telomerase or ALT (alternative lengthening of telomeres) mechanisms maintain telomeres by compensating natural telomeric loss. We have set up a flow-FISH method and using mouse lymphoma cell lines we identified unexpectedly the presence of subpopulations of cells with different telomere lengths. Subpopulations of cells with different telomere lengths were also observed in a human ALT and non-ALT cell line. Differences in telomere length between subpopulations of cells were significant and we term this phenomenon TELEFLUCS (TElomere LEngth FLUctuations in Cell Subpopulations). By applying flow-FISH we could successfully measure telomere lengths during replicative senescence in human primary fibroblasts with different genetic defects that confer sensitivity to ionising radiation (IR). The results from this study, based on flow-FISH and Southern hybridisation measurements, revealed an accelerated rate of telomere shortening in radiosensitive fibroblasts. We also observed accelerated telomere shortening in murine BRCA1 deficient cells, another defect conferring radiosensitivity, in comparison with a BRCA1 proficient cell line. We transiently depleted BRCA1 by siRNAs in two human mammary epithelial cell lines but could not find changes in telomere length in comparison with control cells. Cytological evidence of telomere dysfunction was observed in all radiosensitive cell lines. These results suggest that mechanisms that confer sensitivity to IR may be linked with mechanisms that cause telomere dysfunction. Furthermore, we have been able to show that human ALT positive cell lines show dysfunctional telomeres as detected by either the presence of DSBs at their telomeres or cytogenetic analysis and usually cells with dysfunctional telomeres are sensitive to IR. Finally, we assessed hTERT mRNA splicing variants and telomerase activity in brain tumours, which exhibit considerable chromosome instability suggesting that DNA repair mechanisms may be impaired. We demonstrated that high levels of hTERT mRNAs and telomerase activity correlate with proliferation rate. The presence of hTERT splice variants did not strictly correlate with absence of telomerase activity but hTERT spliced transcripts were observed in some telomerase negative brain tumours suggesting that hTERT splicing may contribute to activation of ALT mechanisms.
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Chen, Yu-Jen, and n/a. "Studies of genes associated with telomere maintenance mechanisms in gliomas." University of Otago. Department of Pathology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080211.155343.

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The overall survival for patients with glioblastoma multiforme (GBM) has not improved in two decades. A better understanding of the molecular basis for gliomagenesis would aid therapeutic advances. Recombinational based alternative lengthening of telomeres (ALT) is a telomere maintenance mechanism (TMM) distinct from telomerase, which serves as a prognostic factor in GBM. In this thesis, I have compared components of the p53 axis, namely p53, p21[WAF-1] and the paired box-containing transcription factors (PAX) PAX2, 5, and 8, with TMM in gliomas. Analysis of TP53 status in relation to TMM in 110 gliomas revealed that activation of ALT during tumorigenesis possibly requires loss of normal TP53 function (P < 0.0001). Overexpression of p21[WAF-1] was also found to correlate with telomerase-positive gliomas (P = 0.0002). Moreover, high p21[WAF-1] expression is a poor prognostic factor in patients under 56 years (P = 0.015). Telomere length (TL) was also found as a prognostic factor, such that short TL (< 5 kb) is a poor prognostic factor in the group without defined TMM ("None")(P = 0.0160). Pax2,5 and 8 belong to Group II of the PAX family. They are expressed at the midbrain-hindbrain boundary (MHB) and in the neural tube of the vertebrate embryo, whereas their expression levels are low in the adult brain. To explore their roles in glioma pathology, I analyzed mRNA levels in 54 gliomas and 16 established glioma cell lines. Increased levels of PAX8 mRNA were detected in 74.1% of gliomas and 62.5% of established glioma cell lines by real time PCR. Sixty-six percent of glioma specimens expressed high levels of active PAX2, 5, and 8 by immunohistochemistry. There were more males than females having high PAX2 expression (P = 0.0408). Suppression of PAX8 by small interfering RNA induced glioma cell death, independent of TP53 status. These findings identify PAX8 as a survival factor for GBM, and PAX2, 5, and 8 expression as contributing to the aggressive behavior of gliomas. The mRNA level of PAX8 showed a positive correlation with telomerase activity in glioma biopsies (r� = 0.75, P < 0.001). The relationship was explored and I found that PAX2 and PAX8 are able to activate the reporter constructs of both the catalytic subunit (hTERT) and the RNA component (hTR) of telomerase. PAX8 had a stronger effect than PAX2 on the activation of the hTERT and hTR promoters. By electrophoretic mobility shift assay, Western blotting and telomerase activity assay, I showed that PAX8 bound directly to hTERT and hTR promoters, and upregulated hTERT protein and telomerase activity. Moreover, gliomas carrying wild type TP53 had higher levels of PAX8 expression compared to those with mutant TP53 (P = 0.0075) suggesting that PAX8 is significant only in some GBMs during gliomagenesis. These results show that the oncofetal proteins, PAX2 and PAX8, may have roles in telomerase regulation. Taken together, molecular markers examined in this thesis suggest gliomas with different TMMs are derived from different pathways.
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Kargaran, Kobra. "The role of BRCA1 in telomere maintenance." Thesis, Brunel University, 2015. http://bura.brunel.ac.uk/handle/2438/13671.

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Telomeres are fundamental structures found at the end of all eukaryotic chromosomes that function to protect the end of chromosomes from end-to-end fusion, erosion and subsequent telomere dysfunction. Telomerase and alternative lengthening of telomere (ALT) mechanisms maintain the telomeres by compensating natural telomeric loss. ALT is found to be present in 15% of human tumours lines and it may be expressed at low levels in the normal mouse tissues. However, the exact mechanism behind ALT depression and/or activation in the mammalian cells is not fully understood. Previous studies have highlighted the role of BRCA1 in telomere dysfunction. Also, it has recently been shown that BRCA1 co-localises at telomeres in the ALT + human cells through BLM and Rad50. However, it is still unclear whether BRCA1 plays a direct role on telomere length maintenance and integrity. The aim of this project was to examine the role of BRCA1 in telomere maintenance associate with ALT in BRCA1 defective mammalian cells. Therefore to achieve this, we have set up series of experiments to look at, (a) hallmarks of ALT activity at the cytological level, (b) measuring of ALT activity using biochemical and immunocytochemistry techniques and (c) understanding the role of BRCA1 in DNA damage response mechanism and telomere dysfunction. Firstly, we found elevated levels of recombination at telomeres in the two human BRCA1 carrier cell lines and mouse embryonic stem cell with deficiency in Brca1-/-. Secondly, our data showed that human and mouse BRCA1 defective cells are significantly more sensitive to ionizing radiation in line with the DNA repair function of BRCA1. Moreover, we found persistent DNA damage at telomeres in the BRCA1 defective environment when after exposure of cells to ionizing radiation. Thirdly, we found evidence of ALT activity in some mouse cell lines, and elevated ALT in mouse cells defective in Brca1. Finally, we examined some other ALT markers using immunofluorescence. Our data indicate differences between human and mouse cells in regulating ALT. Taken together data presented in this thesis revealed that (i) BRCA1 plays a major role in telomere maintenance and defective BRCA1 mammalian cells show evidence of telomere dysfunction and telomere length shortening in line with previous publish data, (ii) BRCA1 defective mouse cells have elevated levels of ALT, (iii) the mouse lymphoblastoid LY-S cells have complete absence of ALT.
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Martinez, Alaina R. "Variant requirements for DNA repair proteins in cancer cell lines that use alternative lengthening of telomere mechanisms of elongation." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1479924417740462.

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Poos, Alexandra Maria [Verfasser], and Karsten [Akademischer Betreuer] Rippe. "Mixed Integer Linear Programming based approaches to study telomere maintenance mechanisms / Alexandra Maria Poos ; Betreuer: Karsten Rippe." Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1206733985/34.

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Poos, Alexandra [Verfasser], and Karsten [Akademischer Betreuer] Rippe. "Mixed Integer Linear Programming based approaches to study telomere maintenance mechanisms / Alexandra Maria Poos ; Betreuer: Karsten Rippe." Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1206733985/34.

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Books on the topic "Telomeres maintenance mechanism"

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A. Morrish, Tammy, ed. Telomerase and non-Telomerase Mechanisms of Telomere Maintenance. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.73734.

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Book chapters on the topic "Telomeres maintenance mechanism"

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Vasianovich, Yulia, Alexandra Krallis, and Raymund Wellinger. "Telomerase in Space and Time: Regulation of Yeast Telomerase Function at Telomeres and DNA Breaks." In Telomerase and non-Telomerase Mechanisms of Telomere Maintenance. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.85750.

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Nag, Snehasish. "Syndromes Associated with Telomere Shortening." In Telomerase and non-Telomerase Mechanisms of Telomere Maintenance. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.88792.

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Audry, Julien, and Kurt W. Runge. "Telomere Formation Systems in Budding and Fission Yeasts." In Telomerase and non-Telomerase Mechanisms of Telomere Maintenance. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.86176.

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Jirkovská, Marie, Marie Korabečná, and Soňa Laššáková. "Telomeres and Telomerase Activity in the Human Placenta." In Telomerase and non-Telomerase Mechanisms of Telomere Maintenance. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.86327.

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Singh Yadav, Prem, and Abubakar Muhammad Wakil. "Telomerase Structure and Function, Activity and Its Regulation with Emerging Methods of Measurement in Eukaryotes." In Telomerase and non-Telomerase Mechanisms of Telomere Maintenance. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89506.

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Capkova, Radmila, and James M. "Telomeres: Their Structure and Maintenance." In The Mechanisms of DNA Replication. InTech, 2013. http://dx.doi.org/10.5772/51356.

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J., Matthew, and Dominique Broccoli. "Telomere Maintenance Mechanisms in Soft Tissue Sarcomas." In Soft Tissue Tumors. InTech, 2011. http://dx.doi.org/10.5772/26996.

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Conference papers on the topic "Telomeres maintenance mechanism"

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Heaphy, Christopher M., Michael C. Haffner, and Alan K. Meeker. "Abstract A06: A novel cell line model of the alternative lengthening of telomeres (ALT) telomere maintenance mechanism." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-a06.

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Graham, Mindy K., Jacqueline Brosnan-Cashman, Anthony Rizzo, Michael Haffner, Alan Meeker, and Christopher Heaphy. "Abstract 4767: Generating and characterizing novel prostate cancer cell lines that employ the alternative lengthening of telomeres (ALT) telomere maintenance mechanism." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4767.

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Gocha, April R. S., Gerard J. Nuovo, and Joanna Groden. "Abstract B57: Coexistence of telomerase-dependent and -independent telomere maintenance mechanisms in human osteosarcoma tumors." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-b57.

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Lopez, Gonzalo, Karina Conkrite, Kendra Hong, Jo Lynne Harenza, John M. Maris, and Sharon Diskin. "Abstract 4881: Dissecting telomere maintenance mechanisms in neuroblastoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4881.

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Sampl, Sandra, Juliane Hadolt, Philip Kienzl, Tamara Braunschmid, Stefan Stättner, Jeremy D. Henson, Roger R. Reddel, Brigitte Marian, and Klaus Holzmann. "Abstract 4597: Telomere maintenance mechanism and expression in colorectal cancer." 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.am2012-4597.

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Robinson, Nathaniel J., Derek J. Taylor, and William P. Schiemann. "Abstract 112: Telomere proteins coordinate intracellular signaling to control telomere maintenance mechanism selection and metastatic recurrence." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-112.

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Barthel, Floris P., Siyuan Zheng, and Roel G. Verhaak. "Abstract 3468: Comprehensive analysis of telomere length and telomere maintenance mechanisms across 31 human cancer types." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3468.

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Medves, Sandrine, Morgan Auchter, Laetitia Chambeau, Sophie Gazzo, Aurélie Verney, Etienne Moussay, Wim Ammerlaan, et al. "Abstract 4055: Non-canonical telomere maintenance mechanism in B-cell chronic lymphocytic leukemia." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4055.

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