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Dissertations / Theses on the topic 'Alternative lengthening of telomeres (ALT)'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Lu, Robert. "The FANCM-BLM-TOP3A-RMI1/2 complex suppresses telomere replication stress and Alternative Lengthening of Telomeres." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23414.

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In humans, telomeres consist of ′TTAGGG′ repeats, which form a nucleoprotein complex that caps the ends of chromosomes. Telomeres are constitutively bound by a six-member protein complex called shelterin. The telomere nucleoprotein structure is essential for preventing the recognition of chromosome ends as DNA double-strand breaks, and for suppressing aberrant repair processes, including end-joining and recombination. When telomeres become critically short, they can initiate a DNA damage response, thereby triggering replicative senescence. Cancer cells are able to overcome this proliferative b

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12

Braun, Delia [Verfasser], and Karsten [Akademischer Betreuer] Rippe. "Inducing and suppressing the alternative lengthening of telomeres mechanism in cancer cells / Delia Braun ; Betreuer: Karsten Rippe." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1199939382/34.

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13

Misino, Stefano [Verfasser]. "Towards a mechanistic understanding of the role of TERRA in the alternative lengthening mechanism of telomeres / Stefano Misino." Mainz : Universitätsbibliothek der Johannes Gutenberg-Universität Mainz, 2021. http://d-nb.info/1241739560/34.

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14

Novo, Clara Patrícia Lopes. "Investigation of the mechanism that underlies MS32 minisatellite instability in cells that use the alternative lengthening of telomeres pathway." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/10211.

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Cancer cells escape senescence by activating a telomere maintenance mechanism (TMM) to elongate telomeres and continue dividing. The most common TMM is the enzyme telomerase that adds telomeric repeats. However, some cancer cells activate the Alternative Lengthening of Telomeres (ALT), a recombination-based mechanism to extend shortened telomeres. One of the most peculiar features of ALT+ cells is the instability at the MS32 minisatellite (D1S8), especially as six other minisatellites remained stable in these cells. As MS32 instability correlates with activation of the ALT mechanism, it is lik

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15

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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16

Anjomani, Virmouni Sara. "Genotype and phenotype characterisation of Friedreich ataxia mouse models and cells." Thesis, Brunel University, 2013. http://bura.brunel.ac.uk/handle/2438/7831.

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Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disorder, caused by a GAA repeat expansion mutation within intron 1 of the FXN gene, resulting in reduced level of frataxin protein. Normal individuals have 5 to 40 GAA repeat sequences, whereas affected individuals have approximately 70 to more than 1000 GAA triplets. Frataxin is a mitochondrial protein involved in iron-sulphur cluster and heme biosynthesis. The reduction in frataxin expression leads to oxidative stress, mitochondrial iron accumulation and consequential cell death with the primary sites of neurons of the dor

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17

Neumayer, Bettina [Verfasser], and Bence [Akademischer Betreuer] Sipos. "Loss of DAXX/ATRX expression and alternative lengthening of telomeres in insulinomas and neuroendocrine tumours of the small intestine / Bettina Neumayer ; Betreuer: Bence Sipos." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1163462187/34.

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18

Jeitany, Maya. "Les mécanismes ALTernatifs de maintenance des télomères dans les cellules souches de gliome." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T010/document.

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Les cellules souches de gliomes (CSG), une sous-population de cellules tumorales, seraient en partie responsables de l’échec des traitements des gliomes de par leur résistance et leur capacité régénérative. Le mécanisme alternatif (ALT) de maintenance des télomères, basé sur la recombinaison homologue et non pas sur la télomérase, est détecté dans environ 30% des gliomes humains suggérant que des stratégies thérapeutiques spécifiquement dirigées contre ALT pourraient avoir un intérêt thérapeutique. Dans ce travail, nous avons poursuivi la caractérisation du premier exemple de CSG humaines ayan

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19

Burkert, Christian Martin. "Cis-regulation and genetic control of gene expression in neuroblastoma." Doctoral thesis, Humboldt-Universität zu Berlin, 2021. http://dx.doi.org/10.18452/23008.

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Genregulation beeinflusst Phänotypen im Kontext von Gesundheit und Krankheit. In Krebszellen regulieren genetische und epigenetische Faktoren die Genexpression in cis. Das Neuroblastom ist eine Krebserkrankung, die häufig im Kindesalter auftritt. Es ist gekennzeichnet durch eine geringe Anzahl exonischer Mutationen und durch häufige Veränderungen der somatischen Kopienzahl, einschließlich Genamplifikationen auf extrachromosomaler zirkulärer DNA. Bisher ist wenig darüber bekannt, wie lokale genetische und epigenetische Faktoren Gene im Neuroblastom regulieren. In dieser Arbeit kombiniere ich di

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20

Terranova, Katherine. "Defining RAD54 function in the alternative lengthening of telomeres pathway." Thesis, 2020. https://hdl.handle.net/2144/41737.

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BACKGROUND: Telomeres are the DNA sequences at the end of chromosomes that are made up of highly repetitive sequences to protect the ends of chromosomes from damage. Telomeres shorten with each round of DNA replication eventually causing cellular senescence. Many cancer cells are able to overcome or evade senescence by elongating their telomeres. Alternative lengthening of telomeres (ALT) is a recombination based mechanism used by cancer cells to maintain telomere length. Evidence supports that unresolved replication stress at telomeric DNA promotes telomere elongation. Given the role of

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21

Cox, Kelli. "Replication stress and the alternative lengthening of telomeres pathway." Thesis, 2016. https://hdl.handle.net/2144/16743.

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In an effort to achieve replicative immortality, human cancer cells must avoid the constant telomere attrition that accompanies DNA replication. Cancer cells accomplish this by employing mechanisms to lengthen their telomeres. Approximately 10 percent of all cancers utilize the Alternative Lengthening of Telomeres (ALT) pathway to maintain telomere length. Although ALT is known to rely on homologous recombination between two telomeric sequences, the exact mechanism and regulators of the ALT pathway remain elusive. As common fragile sites, telomeres pose a challenge to the replication machiner

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22

Al, Murshedi Fathiya. "Role of FANCM in Alternative Lengthening of Telomeres (ALT) Human Cells." Thesis, 2010. http://hdl.handle.net/1807/24237.

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Most immortal human cells maintain their telomeres by up-regulating the enzyme telomerase. Approximately 10-15% of immortal cells maintain their telomere lengths by a recombination-based mechanism termed alternative lengthening of telomeres (ALT). Human ALT cells are characterized by ALT associated promyelocytic bodies (APBs) that contain proteins involved in DNA damage response and repair. Our lab has found significant colocalization of several components of the Fanconi Anemia (FA) pathway with telomeres and demonstrated that knockdown of FANCD2 leads to ALT-specific increase in the amount of

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23

Salgado, Sara Barros. "Exploring the roles of PC4 in the Alternative Lengthening of Telomeres pathway." Master's thesis, 2022. http://hdl.handle.net/10362/130700.

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Telomeres are nucleic acids-protein complexes located at the ends of linear eukaryotic chromosomes comprising 5’-TTAGGG-3’ tandem repeats, the multiprotein complex shelterin and the long non-coding RNA TERRA. Telomeres act both as molecular clocks and capping structures supporting chromosome integrity. Due to the end-replication problem, telomeres progressively shorten with each cell division and ultimately trigger cellular senescence. Cancer cells bypass senescence and divide indefinitely by activating mechanisms that buffer telomere shortening. Most cancers reactivate the reverse transcript

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24

Root, Heather. "The Fanconi Anaemia Protein D2 has an Essential Role in Telomere Maintenance in Cells that Utilize the Alternative Lengthening of Telomeres Pathway." Thesis, 2010. http://hdl.handle.net/1807/26231.

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Fanconi anaemia (FA) is an inherited disorder characterized by bone marrow failure, cancer predisposition and congenital abnormalities. The 12 known FA genes have been implicated in homologous recombination (HR), a process involved in telomere maintenance. A complex of at least 7 FA proteins promotes FANCD2 monoubiquitination and nuclear foci formation. FANCD2 colocalizes and interacts with HR proteins, however the role of FANCD2 in HR is unclear. Telomeres in dividing human somatic cells shorten until they reach a critical length, triggering most cells to undergo senescence or apoptosis. Rar

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25

Komosa, Martin. "The Fanconi Anaemia Protein FANCJ is Involved in the Alternative Lengthening of Telomeres (ALT) Mechanism in Human Cells." Thesis, 2011. http://hdl.handle.net/1807/29580.

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Approximately 15% of human cancers utilize a recombination-based mechanism termed Alternative Lengthening of Telomeres (ALT) to maintain the lengths of their telomeres. The Fanconi anaemia protein FANCJ localizes to telomeric foci in human ALT cells, but not in telomerase-positive or primary cells. Telomere-associated FANCJ frequently localizes with FANCD2 and BRCA1, and primarily localizes to ALT-associated PML nuclear bodies. Depletion of FANCJ in human ALT cells causes the loss of BRCA1 at telomeric foci and a decrease in telomeric repeat DNA content primarily as a result of the loss of the

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26

Mason-Osann, Emily. "Defining mechanisms that regulate the alternative lengthening of telomeres." Thesis, 2020. https://hdl.handle.net/2144/39411.

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Telomeres are repetitive DNA sequences found at the ends of eukaryotic chromosomes that help maintain genome stability. Telomeres shorten every time a cell divides, eventually inducing replicative senescence. To gain replicative immortality cancer cells establish mechanisms to maintain telomere length over many cell divisions. Around 10% of cancers do this using a recombination-based pathway called the Alternative Lengthening of Telomeres (ALT). ALT resembles a specific type of homology-directed repair called break-induced replication (BIR). Through this body of work, we aimed to better unders

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27

Liau, Jau-Yu, and 廖肇裕. "Alternative Lengthening of Telomeres and Loss of ATRX/DAXX Expression in Sarcomas with Clinicopathological Features." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/k88g63.

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博士<br>國立臺灣大學<br>病理學研究所<br>106<br>Alternative lengthening of telomeres (ALT) is a telomerase-unrelated telomere maintenance mechanism that maintain the cell division ability in cancer cells. Currently it is supposed that homologous recombination and DNA repair are utilized in this mechanism, which copy the telomeres and other DNA sequences from other chromosomes to maintain the telomere length. ALT positive cells are characterized by telomere length heterogeneity and some chromosomes may have extremely long telomeres. These phenomena can be visualized by Southern blotting or telomere fluorescen

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28

Larsen, Andrew. "Characterizing the Organization within Alternative Lengthening of Telomere Associated-promyelocytic Leukemia Nuclear Bodies." Thesis, 2010. http://hdl.handle.net/1807/25743.

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In the absence of telomerase activity, a subset of cancerous and immortalized cells maintain telomere length by means of a poorly understood mechanism, termed alternative lengthening of telomeres (ALT). Many details of telomere maintenance in ALT positive cells remain unclear, but significant evidence implicates a homologous recombination mechanism. ALT specific nuclear structures, known as ALT-associated promyelocytic leukemia nuclear bodies (APBs), are thought to serve as the site of telomere extension. Using electron spectroscopic imaging we have demonstrated that APBs contain substantial a

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