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Dissertations / Theses on the topic 'Kaposi's sarcoma'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Kimball, Louise Elizabeth. "Humoral immune response to Kaposi's sarcoma-associated herpesvirus in persons with and without Kaposi's sarcoma /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9284.

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2

Wiggins, Charles Lamar. "Kaposi's sarcoma and sexually transmitted disease /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/10933.

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3

Whitby, Denise. "Human herpesvirus 8 (HHV-8) and Kaposi's sarcoma." Thesis, Institute of Cancer Research (University Of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368195.

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4

Kubo, Toru. "Human immune responses against Kaposi's Sarcoma-associated Herpesvirus (KSHV)." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429041.

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5

Malik, Poonam. "The multifunctional ORF57 protein of Kaposi's sarcoma-associated herpesvirus." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400755.

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6

Mayama, Satoshi. "Seroprevalence and molecular epidemiology of Kaposi's sarcoma-associated herpesvirus." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405058.

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7

Pozniak, Anton Louis. "HIV-related tuberculosis and pulmonary Kaposi's Sarcoma in Zimbabwe." Thesis, University of Bristol, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241119.

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8

Durrington, Hannah Jane. "Kaposi's sarcoma-associated herpesvirus and bone morphogenetic protein signalling." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608400.

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9

Wakeham, Katie. "The epidemiology of Kaposi's sarcoma associated-herpesvirus in Uganda." Thesis, University of York, 2013. http://etheses.whiterose.ac.uk/4518/.

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Over the past two decades there has been an explosion in the number of cases of Kaposi’s sarcoma (KS) in parts of sub-Saharan Africa, where Kaposi’s sarcoma associated-herpesvirus (KSHV) and HIV are relatively prevalent. Currently KS is the most commonly reported cancer in Uganda causing significant morbidity and mortality. Limiting KSHV transmission or halting disease progression could prevent KS. Here, I describe an investigation of factors that might impact on transmission of KSHV and report the first prospective study of antibody titre to KSHV to determine risk of KS from Africa. Stored sa

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10

Owen, Christopher Bradley. "Utilising omics approaches to understand Kaposi's sarcoma-associated herpesvirus." Thesis, University of Leeds, 2015. http://etheses.whiterose.ac.uk/11782/.

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Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic human virus associated with a number of malignancies, including Kaposi’s sarcoma. Similar to all herpesviruses, KSHV establishes either latent or lytic infections in host cells. The latent stage involves minimal viral gene expression, enabling the virus to remain dormant, maintaining genome integrity and enabling viral persistence. Conversely, lytic replication is characterised by the expression of a highly regulated and coordinated cascade of viral gene expression, ultimately resulting in the production of new mature, infectious v

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11

Sodhi, Akrit. "The Kaposi's sarcoma associated herpesvirus : a model for viral oncogenesis /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2005. http://uclibs.org/PID/11984.

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12

Elzinger, Bianca Ariane. "Studies on a new human herpesvirus, Kaposi's sarcoma-associated herpesvirus." Thesis, University College London (University of London), 2000. http://discovery.ucl.ac.uk/1318064/.

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Kaposi's sarcoma (KS)-associated herpesvirus (KSHV), also called human herpesvirus 8 (HHV8), has been been identified in all epidemiological forms of KS as well as in tissue obtained from primary effusion lymphoma (PEL) and Multicentric Castleman's disease (MCD). The KSHV genome contains several putative oncogenes, suggesting that viral infection may induce cellular transformation and tumorgenesis. Herpesviruses encode a number of different surface glycoproteins, which are involved in virus-host interactions. Studies have shown that the viral glycoproteins H and L form a complex that plays an

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13

Turner, Sarah Kistler. "In vivo studies of the Kaposi's sarcoma associated herpesvirus (KSHV)." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251596.

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14

Othman, Zulkefley. "Translational control of Kaposi's sarcoma associated herpesvirus (KSHV) vFlip expression." Thesis, University of Surrey, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616480.

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Kaposi's sarcoma associated herpesvirus (KSHV), is a gammaherpesvirus from the Herpesviridae family and causes a number of proliferative diseases such as Kaposi sarcoma, primary effusion lymphoma and Castleman disease. The prime effectors of the cell proliferation occurring during KSHV infections are the latent gene products LANA, vCyclin and vFLIP. The analysis of the mRNA latent gene transcripts produced by KSHV showed no monocistronic transcript encoding vFLIP suggesting its expression was regulated by a non-canonical translation mechanism. Indeed, previous studies proposed that an IRES ele

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15

Ramos, Heidi C. "Extracellular Matrix-Induced Pathogenic Gene Expression in Kaposi's Sarcoma Herpesvirus (KSHV)." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_theses/148.

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Mechanistic insights on molecular and cellular mechanisms whereby KSHV induces Kaposi?s sarcoma (KS) are key for our understanding of KS tumors and for the development of new therapies. We have previously developed an animal model for KSHV induced KS using murine bone marrow cells transfected with a KSHVBac36. We found that although these cells lacked attributes of transformed cells in vitro, they were able to cause KS-like tumors in vivo. In vivo tumorigenesis correlated with upregulation of both KSHV lytic genes and host angiogenesis suggesting that that cues provided from the microenvironme

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16

Mendoza, Tania Regina Tozetto. "Análise da variabilidade genética do Herpesvirus 8 humano (HHV-8) em indivíduos infectados por HIV com e sem sarcoma de Kaposi." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/99/99131/tde-31012014-111943/.

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O HHV-8 (herpesvírus 8 humano) é o agente etiológico do sarcoma de Kaposi (SK). Diferentemente dos outros herpesvírus, o HHV-8 é distribuído de modo não ubíquo ao redor do mundo. São sete os principais genótipos de HHV-8, de acordo com o padrão de variabilidade da ORF K1: A, B, C, D, E, F e Z. Estudos da variabilidade genética do HHV-8 poderão trazer melhores interpretações sobre o potencial patogênico dos genótipos de HHV-8 e das variações genotípicas funcionais. Dados sobre a variabilidade genética do HHV-8 no Brasil, em que o SK é associado ao HIV, permanecem escassos. Pelo nosso conhecimen

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17

Staudt, Michelle Ruth. "Analysis of the principle latent promoter of Kaposi's sarcoma-associated herpesvirus." Oklahoma City : [s.n.], 2006.

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18

Taylor, Adam. "Functional analysis of Kaposi's Sarcoma-Associated Herpesvirus ORF57 RNA binding motifs." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540582.

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19

Cuomo, Maria Emanuela. "Functional analysis of the cyclin encoded by Kaposi's sarcoma herpes virus." Thesis, Institute of Cancer Research (University Of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397647.

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20

Cook, Rachelle. "Molecular epidemiology of Kaposi's sarcoma-associated herpesvirus in an endemic country." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397652.

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21

Bourboulia, Dimitra. "Humoral and cellular immune responses against Kaposi's sarcoma-associated herpesvirus (KSHV)." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446705/.

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Kaposi's sarcoma-associated herpesvirus (KSHV) is the 8th human herpesvirus discovered in 1994. After primary infection, KSHV establishes latency and, in the context of immunosuppression, has been associated with specific malignancies: Kaposi's sarcoma (KS), primary effusion lymphoma (PEL) and multicentric Castleman's disease (MCD). Seroepidemiological surveys suggest that KSHV is not a ubiquitous virus and several transmission routes and risk factors must exist to explain its global distribution. The increased risk of KSHV-associated cancers in human immunodeficiency virus (HIV)-infected indi

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22

Hollyman, Daniel Royston. "Cellular targets of Kaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446591/.

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The latency-associated nuclear antigen (LANA1) of Kaposi's sarcoma-associated herpesvirus (KSHV) is a multi-function protein involved in maintenance of the viral episome and has been shown to interact with several proteins including p53 and pRB. It is likely that the multifunctional role of LANA1 exceeds these observations therefore the work in this thesis aimed to study LANA1 at both the transcription and protein-protein interaction level. I developed a lentiviral system for the infection of primary endothelial cells with LANA1, to analyse changes in gene expression profiles by gene expressio

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23

Wilson, Sam John. "The reduction and induction of Kaposi's sarcoma-associated herpesvirus lytic replication." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445187/.

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In humans, Kaposi's Sarcoma-associated Herpesvirus (KSHV) is capable of establishing latent infection in B-cells. During latency no infectious virions are produced, the viral episome is maintained and few viral genes are expressed. Latently infected cells, however, retain the capacity to enter the lytic cycle. KSHV ORF50 encodes the transcription factor RTA whose expression is sufficient to initiate the full lytic cycle. RNA interference (RNAi) involves the sequence specific silencing of gene expression. Although extensively validated and widely available at present, lentiviral vector-mediated

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24

Hong, Angela M. "Cell cycle protein expression in AIDS-related and classical Kaposi's sarcoma." Connect to full text, 2004. http://hdl.handle.net/2123/583.

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Thesis (Ph. D.)--University of Sydney, 2004.<br>Title from title screen (viewed 5 May 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Faculty of Medicine. Includes list of published articles and presentations. Includes bibliographical references. Also available in print form.

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25

Hong, Angela Manyin. "Cell cycle protein expression in AIDS-related and classical Kaposi's sarcoma." Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/583.

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Kaposi�s sarcoma (KS) is a peculiar vascular neoplasm that occurs mainly in elderly Mediterranean men and patients with acquired immunodeficiency syndrome (AIDS). The current literature indicates that KS is initiated by the human herpes virus 8 (HHV8) as a reactive polyclonal process but with deregulation of oncogene and tumour suppressor genes, it can progress to a true malignancy with monoclonality. Clinically, classical KS often presents as an indolent disease affecting mainly the lower extremities whereas AIDS-related KS has no site predilection and can progress rapidly with systemi

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26

Hong, Angela Manyin. "Cell cycle protein expression in AIDS-related and classical Kaposi's sarcoma." University of Sydney. Pathology, 2004. http://hdl.handle.net/2123/583.

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Kaposi�s sarcoma (KS) is a peculiar vascular neoplasm that occurs mainly in elderly Mediterranean men and patients with acquired immunodeficiency syndrome (AIDS). The current literature indicates that KS is initiated by the human herpes virus 8 (HHV8) as a reactive polyclonal process but with deregulation of oncogene and tumour suppressor genes, it can progress to a true malignancy with monoclonality. Clinically, classical KS often presents as an indolent disease affecting mainly the lower extremities whereas AIDS-related KS has no site predilection and can progress rapidly with systemi

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27

Pyakurel, Pawan. "AIDS and endemic kaposi's sarcoma development comparison by histopathology, virology (HHV-8/KSHV) and cytogenetics /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-465-1/.

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28

O'Leary, John James. "Molecular analysis of Kaposi's sarcoma associated herpes virus (KSHV) in immunocompromised patients." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360468.

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29

Gould, Faye. "Kaposi's Sarcoma-Associated Herpesvirus RTA Promotes Degradation of Cellular bHLH Transcription Factors." Thesis, University of Leeds, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515337.

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30

Robey, R. C. "Characterising the adaptive T-cell immune response against Kaposi's sarcoma-associated herpesvirus." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19226/.

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Kaposi’s sarcoma-associated herpesvirus (KSHV) is causally related to Kaposi’s sarcoma (KS), the most common malignancy in individuals with untreated HIV/AIDS. Several lines of evidence indicate that KS oncogenesis is associated with loss of T cell-mediated control of KSHV-infected cells. However, the adaptive CD8 and CD4 T-cell responses against KSHV have not been fully characterised. Neither the antigenic repertoire nor the immunodominant targets of CD8 and CD4 KSHV-specific T cells are fully understood, and the phenotypes and functions of these cells remain largely unexplored. To investigat

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31

Isaacs, Thuraya. "Kaposi's sarcoma: Genetic subtypes and clinical correlation in a South African population." Master's thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/25281.

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Human herpes virus 8 (HHV8) is the aetiological agent of all forms of Kaposi's sarcoma (KS). Seven major subtypes (A, B, C, D, E, F, Z) based on genetic variability of open reading frame (ORF)-K1, have been identified. Numerous studies point to differing tumorigenic and pathogenic properties of the HHV8 subtypes. The study objective was to determine the prevalence of the HHV8 subtypes in a cohort of clinical and histologically confirmed KS in Cape Town, South Africa, and analyse associations between the different subtypes, clinico- epidemiological forms and clinical presentation of KS. The cli

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32

Vogel, Abby Jeanne. "Noninvasive imaging techniques as a quantitative analysis of Kaposi's sarcoma skin lesions." College Park, Md.: University of Maryland, 2007. http://hdl.handle.net/1903/7679.

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Thesis (Ph. D.) -- University of Maryland, College Park, 2007.<br>Thesis research directed by: Fischell Dept. of Bioengineering . Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.

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33

O'Hara, Andrea Jayne Dittmer Dirk Peter. "Characterization of cellular and viral microRNAs in Kaposi's sarcoma-associated herpesvirus malignancies." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2462.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.<br>Title from electronic title page (viewed Sep. 3, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum in Genetics and Molecular Biology." Discipline: Genetics and Molecular Biology; Department/School: Medicine.

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34

Delobel, Jean. "Quantification of the adhesion force between individual promyelocytic cells and Kaposi's sarcoma cells using a micropipette technique." Thesis, Georgia Institute of Technology, 1992. http://hdl.handle.net/1853/17853.

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35

Brass, Amanda Francine. "vOX2 - a potential immune regulatory protein involved in Kaposi's sarcoma-associated herpesvirus pathogenesis." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/27246.

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Studies on the viral gene, vOX2, have indicated that this 55kDa glycoprotein has a similar structure to the human CD200, an immunoglobulin superfamily gene, containing two extracellular domains, a single transmembrane region and a short cytoplasmic tail. In order to investigate the potential role of vOX2 in an <i>in vivo </i>system, a novel murid herpesvirus, murine herpesvirus 76 (MHV-76), was utilised. MHV-76 is a natural deletion mutant of murine herpesvirus 68 (MHV-68), lacking four unique genes and eight viral tRNA-like genes from the left end of the MHV-68 genome. This deletion has provi

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36

Payette, Paul J. "Characterization of two Kaposi's sarcoma cell lines and their response to chemotherapeutic agents." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0010/MQ28453.pdf.

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37

Samols, Mark Atienza. "Identification and functional analysis of micro-RNSa encoded by Kaposi's sarcoma-associated herpesvirus." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1181143062.

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38

Dodd, Isabel. "Characterisation of the single-stranded DNA binding protein encoded by Kaposi's sarcoma herpesvirus." Thesis, Cranfield University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421241.

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39

Vallery, Tenaya K. "Functional Studies on Polyadenylated Nuclear RNA in Kaposi's Sarcoma- Associated Herpesvirus-lnfected Cells." Thesis, Yale University, 2019. http://pqdtopen.proquest.com/#viewpdf?dispub=13851924.

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<p> Kaposi's sarcoma-associated herpesvirus (KSHV) is one of the known human cancer viruses, causing Kaposi's sarcoma and primary effusion lymphoma in immunosuppressed patients. Although of medical concern, the mechanisms through which the virus causes cancer remain poorly understood. Researchers speculate that the lytic phase contributes to the development of human cancers by this virus.</p><p> KSHV, like other herpesviruses, is predominantly latent in the human host, but undergoes lytic activation to produce infectious viral particles. In the process, the virus hijacks the host machinery t

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40

Feller, J. Kyle. "Correlation of amplification and expression of the c-myc oncogene in Kaposi's sarcoma." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12373.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>The c-myc proto-oncogene is involved in various cellular processes including cell growth, proliferation, and apoptosis. Overexpression and deregulated expression of the gene have been previously linked to seve

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41

Thomas, Mair. "Natural killer cell evasion by the K5 gene of Kaposi's sarcoma-associated herpesvirus." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612324.

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42

Cannon, M. "A functional analysis of the Kaposi's sarcoma-associated herpesvirus G protein-coupled receptor." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445385/.

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Human herpesvirus-8, or KSHV, was discovered in 1994 and is the causative agent of all forms of Kaposi's sarcoma (KS). It is also associated with two lymphoproliferative disorders: primary effusion lymphoma (PEL) and multicentric Castleman's disease. The KSHV viral chemokine receptor, vGPCR, is a homologue of the IL8 receptors CXCR1 and CXCR2. vGPCR is considered a viral oncogene: it transforms fibroblasts in vitro and enhances growth and longevity of primary endothelial cells. vGPCR signals promiscuously via several heterotrimeric G-protein subtypes and activates the MAP and SAP kinases, the

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43

Wood, Jennifer Jane. "The effect of Kaposi's sarcoma-associated herpesvirus RTA expression upon the cellular proteome." Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/6344/.

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Kaposi’s sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi’s sarcoma (KS). Like all herpesviruses, KSHV has a bi-phasic life cycle, with a dormant latent phase and a productive lytic phase. The switch from viral latency to lytic replication is mediated by the replication and transcription activator protein (RTA). RTA activates KSHV lytic gene expression via direct and indirect binding to lytic promoters. Moreover, it functions as an E3 ubiquitin ligase, actively degrading repressor proteins, such as Hey1, maintaining the virus in the latent state. The first aim of this stu

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44

Kakoola, Dorothy Nalwanga. "Human herpesvirus 8 in Uganda : seroprevalence in blood donors, genome variability and evolution." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366192.

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45

Guo, Wei-Xing. "Regulation of AIDS-related Kaposi's sarcoma cell proliferation by steroid/retinoid and their receptors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ38804.pdf.

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46

Barnard, Suzanne. "An investigation into the interactions between Kaposi's sarcoma-associated herpesvirus and the immune system." Thesis, University of Glasgow, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288902.

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47

Moosa, M. R. "The development of malignancies in renal allograft recipients with special emphasis on Kaposi's sarcoma." Thesis, Stellenbosch : Stellenbosch University, 2002. http://hdl.handle.net/10019.1/53101.

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Thesis (PhD)--Stellenbosch University, 2002.<br>ENGLISH ABSTRACT: Renal transplantation is undoubtedly the best treatment for patients with irreversible renal failure. As a prelude to establishing the nature of malignancies in renal transplant patients we sought to determine factors influencing the outcome of renal transplantation. The survival of renal allografts and of recipients is influenced by a number of demographic, clinical and therapeutic factors. Some of these factors have been better studied than others, and we sought to establish the influence of particular factors on our own

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48

Di, Bartolo Daniel L. "Insights into mechanisms of Kaposi's sarcoma : herpesvirus regulating host cell survival and lytic reactivation /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528418061&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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49

Bridge, G. E. M. "Using Kaposi's sarcoma-associated herpesvirus to elucidate the role of cellular microRNAs in endothelial biology." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1410931/.

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Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic γ-herpesvirus that is the etiologic agent of Kaposi sarcoma (KS). KS is an angioproliferative neoplasm composed of cells of endothelial origin. For the work described in this thesis, KSHV infection of endothelial cells was used as a tractable model to study the role of microRNAs (miRNAs) in endothelial cell biology. Previous work in the laboratory had identified miRNAs which are either upregulated or downregulated upon KSHV infection of lymphatic endothelial cells (LEC). Target prediction analysis of these miRNAs and cross-comparis

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50

Sulaiman, Mariam K. "Structural and functional analysis of the Kaposi's sarcoma-associated herpesvirus vFLIP internal ribosome entry site." Thesis, University of Surrey, 2017. http://epubs.surrey.ac.uk/842513/.

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Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic virus, the etiological agent of Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL). One of the key viral proteins that contribute to tumorigenesis is vFLIP, a viral homolog of the FLICE inhibitory protein. This KSHV protein interacts with the NFκB pathway to trigger the expression of antiapoptotic and proinflammatory genes and ultimately leads to tumor formation. The expression of vFLIP is regulated at the translational level by an internal ribosomal entry site (IRES) element. However, the precise mechanism by which ribosome

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