Relevant bibliographies by topics / Alternative lengthening of telomeres (ALT)

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Academic literature on the topic 'Alternative lengthening of telomeres (ALT)'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Alternative lengthening of telomeres (ALT)"

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Cohn, Marita, Ahu Karademir Andersson, Raquel Quintilla Mateo, and Mirja Carlsson Möller. "Alternative Lengthening of Telomeres in the Budding Yeast Naumovozyma castellii." G3: Genes|Genomes|Genetics 9, no. 10 (2019): 3345–58. http://dx.doi.org/10.1534/g3.119.400428.

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The enzyme telomerase ensures the integrity of linear chromosomes by maintaining telomere length. As a hallmark of cancer, cell immortalization and unlimited proliferation is gained by reactivation of telomerase. However, a significant fraction of cancer cells instead uses alternative telomere lengthening mechanisms to ensure telomere function, collectively known as Alternative Lengthening of Telomeres (ALT). Although the budding yeast Naumovozyma castellii (Saccharomyces castellii) has a proficient telomerase activity, we demonstrate here that telomeres in N. castellii are efficiently maintai
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Udroiu, Ion, and Antonella Sgura. "Alternative Lengthening of Telomeres and Chromatin Status." Genes 11, no. 1 (2019): 45. http://dx.doi.org/10.3390/genes11010045.

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Telomere length is maintained by either telomerase, a reverse transcriptase, or alternative lengthening of telomeres (ALT), a mechanism that utilizes homologous recombination (HR) proteins. Since access to DNA for HR enzymes is regulated by the chromatin status, it is expected that telomere elongation is linked to epigenetic modifications. The aim of this review is to elucidate the epigenetic features of ALT-positive cells. In order to do this, it is first necessary to understand the telomeric chromatin peculiarities. So far, the epigenetic nature of telomeres is still controversial: some auth
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Hou, Kailong, Yuyang Yu, Duda Li, et al. "Alternative Lengthening of Telomeres and Mediated Telomere Synthesis." Cancers 14, no. 9 (2022): 2194. http://dx.doi.org/10.3390/cancers14092194.

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Telomeres are DNA–protein complexes that protect eukaryotic chromosome ends from being erroneously repaired by the DNA damage repair system, and the length of telomeres indicates the replicative potential of the cell. Telomeres shorten during each division of the cell, resulting in telomeric damage and replicative senescence. Tumor cells tend to ensure cell proliferation potential and genomic stability by activating telomere maintenance mechanisms (TMMs) for telomere lengthening. The alternative lengthening of telomeres (ALT) pathway is the most frequently activated TMM in tumors of mesenchyma
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Gauchier, Mathilde, Sophie Kan, Amandine Barral, et al. "SETDB1-dependent heterochromatin stimulates alternative lengthening of telomeres." Science Advances 5, no. 5 (2019): eaav3673. http://dx.doi.org/10.1126/sciadv.aav3673.

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Alternative lengthening of telomeres, or ALT, is a recombination-based process that maintains telomeres to render some cancer cells immortal. The prevailing view is that ALT is inhibited by heterochromatin because heterochromatin prevents recombination. To test this model, we used telomere-specific quantitative proteomics on cells with heterochromatin deficiencies. In contrast to expectations, we found that ALT does not result from a lack of heterochromatin; rather, ALT is a consequence of heterochromatin formation at telomeres, which is seeded by the histone methyltransferase SETDB1. Heteroch
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Zhao, Shuang, Feng Wang, and Lin Liu. "Alternative Lengthening of Telomeres (ALT) in Tumors and Pluripotent Stem Cells." Genes 10, no. 12 (2019): 1030. http://dx.doi.org/10.3390/genes10121030.

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A telomere consists of repeated DNA sequences (TTAGGG)n as part of a nucleoprotein structure at the end of the linear chromosome, and their progressive shortening induces DNA damage response (DDR) that triggers cellular senescence. The telomere can be maintained by telomerase activity (TA) in the majority of cancer cells (particularly cancer stem cells) and pluripotent stem cells (PSCs), which exhibit unlimited self-proliferation. However, some cells, such as telomerase-deficient cancer cells, can add telomeric repeats by an alternative lengthening of the telomeres (ALT) pathway, showing telom
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Xu, Mafei, Jun Qin, Leiming Wang, et al. "Nuclear receptors regulate alternative lengthening of telomeres through a novel noncanonical FANCD2 pathway." Science Advances 5, no. 10 (2019): eaax6366. http://dx.doi.org/10.1126/sciadv.aax6366.

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Alternative lengthening of telomeres (ALT) is known to use homologous recombination (HR) to replicate telomeric DNA in a telomerase-independent manner. However, the detailed process remains largely undefined. It was reported that nuclear receptors COUP-TFII and TR4 are recruited to the enriched GGGTCA variant repeats embedded within ALT telomeres, implicating nuclear receptors in regulating ALT activity. Here, we identified a function of nuclear receptors in ALT telomere maintenance that involves a direct interaction between COUP-TFII/TR4 and FANCD2, the key protein in the Fanconi anemia (FA)
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Perrem, Kilian, Lorel M. Colgin, Axel A. Neumann, Thomas R. Yeager, and Roger R. Reddel. "Coexistence of Alternative Lengthening of Telomeres and Telomerase in hTERT-Transfected GM847 Cells." Molecular and Cellular Biology 21, no. 12 (2001): 3862–75. http://dx.doi.org/10.1128/mcb.21.12.3862-3875.2001.

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ABSTRACT It has been shown previously that some immortalized human cells maintain their telomeres in the absence of significant levels of telomerase activity by a mechanism referred to as alternative lengthening of telomeres (ALT). Cells utilizing ALT have telomeres of very heterogeneous length, ranging from very short to very long. Here we report the effect of telomerase expression in the ALT cell line GM847. Expression of exogenous hTERT in GM847 (GM847/hTERT) cells resulted in lengthening of the shortest telomeres; this is the first evidence that expression of hTERT in ALT cells can induce
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Mentegari, Elisa, Federica Bertoletti, Miroslava Kissova та ін. "A Role for Human DNA Polymerase λ in Alternative Lengthening of Telomeres". International Journal of Molecular Sciences 22, № 5 (2021): 2365. http://dx.doi.org/10.3390/ijms22052365.

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Telomerase negative cancer cell types use the Alternative Lengthening of Telomeres (ALT) pathway to elongate telomeres ends. Here, we show that silencing human DNA polymerase (Pol λ) in ALT cells represses ALT activity and induces telomeric stress. In addition, replication stress in the absence of Pol λ, strongly affects the survival of ALT cells. In vitro, Pol λ can promote annealing of even a single G-rich telomeric repeat to its complementary strand and use it to prime DNA synthesis. The noncoding telomeric repeat containing RNA TERRA and replication protein A negatively regulate this activ
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Sung, Ji-Yong, Hee-Woong Lim, Je-Gun Joung, and Woong-Yang Park. "Pan-Cancer Analysis of Alternative Lengthening of Telomere Activity." Cancers 12, no. 8 (2020): 2207. http://dx.doi.org/10.3390/cancers12082207.

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Alternative lengthening of telomeres (ALT) is a telomerase-independent mechanism that extends telomeres in cancer cells. It influences tumorigenesis and patient survival. Despite the clinical significance of ALT in tumors, the manner in which ALT is activated and influences prognostic outcomes in distinct cancer types is unclear. In this work, we profiled distinct telomere maintenance mechanisms (TMMs) using 8953 transcriptomes of 31 different cancer types from The Cancer Genome Atlas (TCGA). Our results demonstrated that approximately 29% of cancer types display high ALT activity with low tel
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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 (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 mu
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Dissertations / Theses on the topic "Alternative lengthening of telomeres (ALT)"

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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
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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 an
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Perrem, Kilian Thomas. "Molecular Studies of an alternative lengthening of telomeres (ALT) mechanism." Thesis, The University of Sydney, 2001. http://hdl.handle.net/2123/793.

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Telomeres are specialised structures, consisting of TTAGGG DNA repeats and binding proteins, that cap the ends of human chromosomes and maintain chromosome integrity. It has been shown that telomeres shorten with each round of cell division in most normal human somatic cells. It has become generally accepted that this shortening is due, in part, to the inability of DNA polymerases to replicate the extreme ends of chromosomes which is a phenomenon known as the 'end replication problem'. An intriguing hypothesis that has emerged from these observations is that critically shortened telomere
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Perrem, Kilian Thomas. "Molecular Studies of an alternative lengthening of telomeres (ALT) mechanism." University of Sydney. Children's Medical Research Institute, 2001. http://hdl.handle.net/2123/793.

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Telomeres are specialised structures, consisting of TTAGGG DNA repeats and binding proteins, that cap the ends of human chromosomes and maintain chromosome integrity. It has been shown that telomeres shorten with each round of cell division in most normal human somatic cells. It has become generally accepted that this shortening is due, in part, to the inability of DNA polymerases to replicate the extreme ends of chromosomes which is a phenomenon known as the �end replication problem�. An intriguing hypothesis that has emerged from these observations is that critically shortened telomere
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Eid, Rita. "A la recherche des effets de l'inactivation génétique d'ATRX dans le déclenchement de la voit ALT (télomérase-indépendante) de maintenance des télomères dans les cellules cancéreuses." Thesis, Tours, 2015. http://www.theses.fr/2015TOUR4021/document.

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Des mutations dans ATRX, une protéine de remodelage de la chromatine, ont été associées, dans plusieurs études cliniques, avec la voie télomérase-indépendante de maintenance des télomères (voie ALT) dans plusieurs types de cancer. Grâce à des expériences d’immunoprécipitation de chromatine (ChIP), nous avons montré qu’ATRX était localisée au niveau subtélomérique de cellules tumorales humaines en culture. Nous avons également montré, par ChIP, que l’inactivation génétique d’ATRX provoquait une diminution des quantités de cohésine/SMC1 présentes dans les régions subtélomériques. L’inactivation
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Mangosh, Tawna L. "SLX4 Interacting Protein (SLX4IP): A Vital Primer for Alternative Lengthening of Telomere (ALT)-like Processes Promoting Replicative Immortality in Castration-resistant Prostate Cancer with Androgen Receptor Loss." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1623255136624147.

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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 c
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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 recombi
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LILLARD, KATHERINE L. "THE BLM HELICASE FUNCTIONS IN ALTERNATIVE LENGTHENING OF TELOMERES." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1097164165.

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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, a
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Book chapters on the topic "Alternative lengthening of telomeres (ALT)"

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Pickett, Hilda A., and Roger R. Reddel. "Alternative Lengthening of Telomeres in Human Cells." In Telomeres and Telomerase in Cancer. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-879-9_5.

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Jiang, Wei-Qin, Jeremy D. Henson, A. Neumann Axel, and R. Reddel Roger. "Protocol III: Detection of Alternative Lengthening of Telomeres." In Telomeres and Telomerase in Cancer. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-879-9_16.

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Azeroglu, Benura, Laurent Ozbun, Gianluca Pegoraro, and Eros Lazzerini Denchi. "Native FISH: A low- and high-throughput assay to analyze the alternative lengthening of telomere (ALT) pathway." In Methods in Cell Biology. Elsevier, 2022. http://dx.doi.org/10.1016/bs.mcb.2022.10.010.

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"Alternative Lengthening of Telomeres." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_210.

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"Alternative Lengthening of Telomeres in Mammalian Cells." In Origin and Evolution of Telomeres. CRC Press, 2008. http://dx.doi.org/10.1201/9781498713498-8.

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Conference papers on the topic "Alternative lengthening of telomeres (ALT)"

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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. "Abstract 3412: Functional knockout ofATRXorDAXXpermits the alternative lengthening of telomeres (ALT) mechanism in prostate cancer cells." 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.am2017-3412.

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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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Malykh, Andrei G., Jonathan R. Doyle, Fang Tian, Joyce HY Lee, Jeremy D. Henson, and Roger R. Reddel. "Abstract 3768: Identification of new alternative lengthening of telomeres (ALT)-positive cancer cell lines using the C-circle assay." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3768.

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Brosnan-Cashman, Jacqueline A., Mindy K. Graham, Anthony J. Rizzo, et al. "Abstract B14: Establishment and characterization of in vitro models of alternative lengthening of telomeres (ALT) in pediatric high-grade glioma." In Abstracts: AACR Special Conference: Pediatric Cancer Research: From Basic Science to the Clinic; December 3-6, 2017; Atlanta, Georgia. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.pedca17-b14.

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Farooqi, Ahsan, Ashly Hindle, Balakrishna Koneru, Jerry Shay, and Patrick Reynolds. "Abstract 580: Increased DNA repair capacities and p53/MDM2 pathway aberrations hallmark neuroblastoma cell lines with the alternative lengthening of telomeres (ALT) phenotype." 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.am2013-580.

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Brosnan-Cashman, Jacqueline A., Christopher M. Heaphy, and Alan K. Meeker. "Abstract 1467: Isolation and characterization of cancer cells containing ultrabright telomere DNA foci associated with alternative lengthening of telomeres (ALT): A novel utility for combined telomere-specific FISH and flow cytometry (Flow FISH)." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1467.

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Barry, Walter, Christopher Heaphy, and Alan Meeker. "Abstract 3470: The promyelocytic leukemia (PML) protein modulates rate and localization of homologous recombination in human cell lines with the alternative lengthening of telomeres (ALT) pathway." 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.am2017-3470.

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Laroche-Clary, Audrey, Vanessa Chaire, Andrei Malykh, Marie Paule Algeo, François Le Loarer, and Antoine Italiano. "Abstract LB-086: ATR inhibition broadly sensitizes TP53-deficient soft-tissue sarcomas to chemotherapy independent of alternative lengthening telomere (ALT) status: Moving forward to personalized medicine." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-086.

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Driest, Kathryn E., Joshua J. Waterfall, Robert L. Walker, et al. "Abstract 2717: Reintroduction of DAXX suppresses alternative lengthening of telomeres in osteosarcoma." 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.am2016-2717.

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Reports on the topic "Alternative lengthening of telomeres (ALT)"

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

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