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Dissertations / Theses on the topic 'JAK/STAT Signaling Pathway'

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Published: 4 June 2021

Last updated: 9 February 2022

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1

Saharinen, Pipsa. "Signaling through the Jak-Stat pathway : regulation of tyrosine kinase activity." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/saharinen/.

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2

Lukashova, Viktoria. "Involvement of the Jak/STAT pathway in platelet-activating factor receptor signaling." Thèse, Sherbrooke : Université de Sherbrooke, 2003. http://savoirs.usherbrooke.ca/handle/11143/4173.

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3

Giedt, Michelle Suzanne. "JAK/STAT SIGNALING REGULATES GAMETOGENESIS AND AGE-RELATED REPRODUCTIVE MAINTENANCE." UKnowledge, 2018. https://uknowledge.uky.edu/biology_etds/52.

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Cell signaling is central to integration of internal and external cues that regulate development and homeostasis. Most development is thought of as pre-adult, but limited developmental processes occur in adults. Gametogenesis incorporates elements of both these facets, with a distinct developmental plan for gamete synthesis which is regulated by integration of homeostatic inputs such as nutrient status, and environmental cues. Signaling pathways integrate and transduce information from these cues to evoke a response. A decline in homeostasis and subsequent cues occurs over time, in the case of

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4

Leal, Cervantes Ana Irene. "Transcriptional consequences of Jak-Stat signalling in haematopoiesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709253.

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5

Kalymbetov, Anuar [Verfasser]. "Role of JAK/STAT signalling pathway in PAH / Anuar Kalymbetov." Gießen : Universitätsbibliothek, 2016. http://d-nb.info/1120270227/34.

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6

Park-Min, Kyung-Hyun. "The crosstalk between ITAM-associated receptors and Jak-STAT signaling pathways /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1296119161&sid=8&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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7

Guo, Qian. "THE FUNCTION OF Socs GENES IN DROSOPHILA DEVELOPMENT AND SIGNALING PATHWAYS." UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_theses/466.

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The duration and intensity of the JAK/stat signaling must be tightly regulated to prevent excessive transcriptional response and to reset the pathway to receive additional signals. Socs are the largest class of these regulators in mammals. Eight Socs genes have been found in mammals. CIS, and SOCS1-3, the canonical Socs, are transcriptionally activated by and down-regulate the JAK signaling. Socs4-7, the non-canonical Socs, are less studied and their relationship with the JAK/STAT pathway has not been well established. The Drosophila genome encodes three non-canonical Socs homologues, Socs16D,

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8

DiNapoli, Vincent A. "Alterations in JAK/STAT signaling pathway and blood-brain barrier function mechanisms underlying worsened outcome following stroke in the aged rat /." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5142.

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Thesis (Ph. D.)--West Virginia University, 2007.<br>Title from document title page. Document formatted into pages; contains x, 154 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 135-149).

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9

Hamedi, Mojgan. "The expression of Suppressor of Cytokine Signalling (SOCS), JAK-STAT signalling pathway and cytokine profile in Behçet's disease." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8557.

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Behçet’s disease (BD) is a chronic, multi systemic, recurrent vasculitis disease of unknown aetiology. The clinical manifestations are composed of relapsing episodes of recurrent oral ulcers, uveitis, skin lesions and genital ulcers along with musculoskeletal and neurological involvement. Pro-inflammatory cytokines are a key feature of the disease but the triggers for their induction are not well understood and/or controversial. Many cytokines (including IFNγ, IL-12, IL-23, IL-10 and IL-6) activate the JAK-STAT signalling pathway which is negatively regulated by Suppressor of Cytokine Signalli

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10

Collura, Kaitlin Marie. "Palmitoylation-Dependent Regulation of the DLK/JNK/cJun and the GP130/JAK/STAT Retrograde Signaling Pathways." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/426710.

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Biomedical Sciences<br>Ph.D.<br>Palmitoylation is the post-translational addition of the 16-carbon fatty acid palmitate to protein cysteine residues. This process is best known for its roles in targeting proteins to lipid membranes, including both the plasma membrane and vesicles. Palmitoylation occurs in all eukaryotic cells, but appears to be particularly important in neurons, because genetic mutation or loss of several palmitoyl acyltransferases (PATs, the enzymes that catalyze palmitoylation), leads to predominantly neuropathological defects. In addition, a growing number of recent studies

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11

Oshiro, Marc Makoto. "Role of interleukin-6 signaling via the Jak/Stat pathway in human myeloma and effects on mediators of cell survival and proliferation." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/284289.

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Multiple myeloma is a B-cell malignancy characterized by the latent accumulation in bone marrow of monoclonal plasma cells with a low proliferative index and an extended life span. Interleukin-6 (IL-6) is the major survival factor for myeloma tumor cells and induces signaling through the Signal Transducer and Activator of Transcription (STAT) proteins. We report that one STAT family member Stat3, is constitutively activated in bone marrow mononuclear cells from patients with multiple myeloma and in the IL-6-dependent human myeloma cell line, U266. U266 cells are shown to constitutively overexp

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12

Rawlings, Jason Scott. "IDENTIFICATION AND CHARACTERIZATION OF SOCS44A IN DROSOPHILA." UKnowledge, 2004. http://uknowledge.uky.edu/gradschool_diss/268.

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The JAK/STAT pathway is but one of the signal transduction cascades responsible for proper development and homeostasis. Gain-of-function mutations of pathway components are causative agents of several leukemias, highlighting the necessity for proper regulation of signal transduction. Drosophila presents an attractive model to study JAK/STAT signaling because mutations in the pathway behave in an analogous manner. Furthermore, the Drosophila cascade is much simpler as only one of each component required for activation has been characterized; whereas in mammals, there are many ligands, receptors

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13

Garr, Edmund Dzigbordi. "JAK/STAT signalling in the induction of the L-arginine-nitric oxide pathway in macrophages and vascular smooth muscle cells." Thesis, University of Hertfordshire, 2014. http://hdl.handle.net/2299/13825.

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The production of Nitric Oxide (NO) under physiological conditions has beneficial roles in acting as a key signaling component of many biological processes as well as having an anti-microbial effect. However its effects following excess production by the inducible NO pathway is potentially detrimental in the pathogenesis of chronic inflammation including sepsis and several other inflammatory diseases. Understanding the mechanisms that regulate the expression of the inducible nitric oxide synthase (iNOS) responsible for producing the excessive amounts of NO in disease states is therefore critic

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14

Gomes, Guilherme Wataru. "Expressão gênica dos transportadores de membrana ABCB1,ABCG2, SLC22A1 e SLCO1A2 em linhagens celulares tratadas com inibidor comercial da via JAK-STAT." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-16032016-095918/.

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INTRODUÇÃO: A desregulação da via de sinalização JAK-STAT é uma característica marcante das neoplasias mieloproliferativas (NMPs), doenças clonais da célula tronco hematopoética, dentre as quais encontra-se a mielofibrose (MF). Diversos inibidores de JAK foram desenvolvidos para o tratamento da MF e encontram-se em diferentes fases de desenvolvimento clínico. Devido ao seu desenvolvimento recente, pouco se sabe a respeito do papel de transportadores de membrana na farmacocinética desses compostos. Essas proteínas realizam o influxo e efluxo celular de substratos endógenos e xenobióticos, e alt

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15

Kowarsch, Andreas [Verfasser], Hans-Werner [Akademischer Betreuer] Mewes, and Fabian J. [Akademischer Betreuer] Theis. "The impact of microRNAs on signaling pathways : From general perspectives to a computational model of the JAK-STAT pathway / Andreas Kowarsch. Gutachter: Fabian J. Theis. Betreuer: Hans-Werner Mewes." München : Universitätsbibliothek der TU München, 2012. http://d-nb.info/1020056983/34.

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16

Ghafoory, Shima. "Development of a screening assay for inhibitors of inflammation useful against pancreatic cancer." Thesis, Mälardalen University, Mälardalen University, School of Sustainable Development of Society and Technology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-7797.

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<p>Pancreatic cancer is the fourth most lethal cancer and ranks as the eighth most commonly diagnosed cancer worldwide. This is due to its rapid proliferation, strong metastatic potential and its delayed detection. One major risk factor for developing pancreatic cancer is the aggressive inflammatory disease chronic pancreatitis. Chronic inflammation frequently precedes the development of certain pancreatic cancers.</p><p>Inflammation is a protective and necessary process by which the body can alert the immune system of the existence of a wound or infection and mount an immune response to remov

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17

Ng, Dominic Chi Hiung. "Characterizing intracellular signaling mechanisms involved in the progression of cardiac hypertrophy and failure : involvement of JAK/STAT and MAPK pathways." University of Western Australia. Biochemistry and Molecular Biology Discipline Group, 2003. http://theses.library.uwa.edu.au/adt-WU2003.0032.

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[Truncated abstract] The innate ability of the heart to compensate for an increase in workload as a result of disease or injury, through an increase in size and mass is known as cardiac hypertrophy. The hypertrophy of the heart compensates for an increase in workload with an increase in cardiac output. However, excessive hypertrophy can result in cardiac dysfunction and substantially increases the risk of cardiac failure and mortality. The molecular mechanisms that regulate the development of cardiac hypertrophy and cardiac failure are not entirely understood. Traditionally, the G-protein Cou

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18

Zhu, Wei. "Negative regulation of JAK/STAT pathway /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3112843.

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19

Pean, Claire. "JAK-STAT pathway in the control of mycobacterial infections." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/jakstat-pathway-in-the-control-of-mycobacterial-infections(cb788a0d-1c53-4f5c-8513-64c8cb50e08e).html.

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Though mammalian JAKs and STATs have been extensively studied over the past 20 years, many aspects of their in vivo function remain unclear. In particular, their roles in control of infection with pathogens remain murky and confusing. One difficulty in understanding how these pathways regulate inflammation is the presence of complex compensatory mechanisms between the different JAK and STAT proteins. In the Dionne lab, we use the fruit-fly Drosophila melanogaster as a model to study the in vivo functions of the JAK/STAT pathway in mycobacterial infection. Flies contain only one JAK (hop), one

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20

Beirer, Stephan. "Mathematical modelling of the Jak-Stat1 signal transduction pathway." Berlin Logos, 2007. http://deposit.d-nb.de/cgi-bin/dokserv?id=2949679&prov=M&dok_var=1&dok_ext=htm.

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21

Han, Ho-chun, and 韓浩俊. "JAK-STAT pathway as potential target of acute myeloid leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B50534208.

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Acute myeloid leukemia (AML) is a group of heterogeneous diseases characterized by an abnormal increase in myeloblasts. Despite intensive chemotherapy and allogeneic bone marrow transplantation, the treatment outcome of AML remains unsatisfactory, with a cure rate of only about 30%. Therefore, novel therapeutic strategies targeting the pathogenetic pathways of leukemia initiation and progression are needed. Using intracellular phospho-flow analysis with normal bone marrow as reference, we detected an increase in phosphorylated-STAT5 (pSTAT5) in three leukemic cell lines (K562, KG-1 and ML-

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22

Stec, Wojciech. "Molecular analysis of the Drosophila JAK/STAT pathway receptor complex." Thesis, University of Sheffield, 2013. http://etheses.whiterose.ac.uk/4509/.

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The JAK/STAT signalling pathway plays a central role in numerous biological processes contributing to development and maintenance of homeostasis. Drosophila melanogaster offers a conserved JAK/STAT pathway with much lower redundancy. For this reason, the fruit fly was used as a model organism to investigate genetic interactions and functions of the JAK/STAT pathway in the context of the whole organism. However, very little is known regarding the molecular mechanisms governing the Drosophila JAK/STAT pathway. Here, we present a molecular analysis of the sole receptor of the JAK/STAT pathway in

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23

Chen, Qian. "THE INTERACTIONS BETWEEN JAK/STAT SIGNALING LIGANDS IN DROSOPHILA MELANOGASTER." UKnowledge, 2014. http://uknowledge.uky.edu/biology_etds/23.

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The development of multi-cellular organisms requires extensive cell-cell communication to coordinate cell functions. However, only a handful of signaling pathways have emerged to mediate all the intercellular communications; therefore, each of them is under an array of regulations to achieve signaling specificity and diversity. One such signaling pathway is the Janus Kinase/ Signal Transducer and Activator of Transcription (JAK/STAT) pathway, which is the primary signaling cascade responding to a variety of cytokines and growth factors in mammals and involved in many developmental processes. T

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24

Gandhi, Hetvi. "Early events in cytokine receptor signaling." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135614.

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Ligand-activated signal transduction is a process critical to cell survival and function as it serves as a means of communication between the cells and their environment. Endocytosis is generally thought to down-regulate incoming signals by reducing the surface availability of receptors. However, increasing evidence in many systems suggests a notion which is referred to as the „signalling endosome" hypothesis - that endocytosis can also actively contribute to signalling apart from clearance of activated receptors and thereby attenuation of signalling. The functional aspect of signalling endoso

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25

Wright, Victoria M. "Investigating the differential properties of the Drosophila JAK/STAT pathway ligands." Thesis, University of Sheffield, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555230.

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The JAK/STAT signalling cascade in vertebrates is activated in response to multiple cytokines and growth factors. By contrast, the Drosophila genome encodes for only three related JAK/STAT ligands, Upd, Upd2 and Upd3. It is hoped that identifying the differences in signalling stimulated by these three Updlike ligands will ultimately lead to a greater understanding of this disease-related pathway and its roles in development. Here, the analysis of the least well characterised of the Upd-like ligands, Upd3, is described. Upd3 is revealed as a secreted molecule that can activate JAK/STAT signalli

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26

Tang, Lingfeng. "THE JAK/STAT PATHWAY IS REUTILIZED IN DROSOPHILA SPERMATOGENESIS." UKnowledge, 2014. http://uknowledge.uky.edu/biology_etds/27.

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In the Drosophila testis, sperm are derived from germline stem cells (GSCs) which undergo a stereotyped pattern of divisions and differentiation. The somatic cells at the tip of the testis form the hub, which is the niche for both the somatic cyst stem cells (CySCs) and GSCs. The hub expresses Upd, a ligand for the JAK/STAT pathway that has roles in the maintenance of CySCs and GSCs. Male mutants of upd3, another ligand of the JAK/STAT pathway, become sterile much earlier than the wild-type, leading to the hypothesis that similar to upd, upd3 also promotes the self-renewal of stem cells in tes

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27

Ning, Shunbin, and Ling Wang. "Inactivation Of Type I IFN Jak-STAT Pathway In EBV Latency." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/6533.

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Epstein-Barr Virus (EBV) latent infection is associated with a variety of lymphomas and carcinomas. Interferon (IFN) Regulatory Factors (IRFs) are a family of transcription factors, among which IRF7 is the “master” regulator of type I IFNs (IFN-I) that defends against invading viruses. Robust IFN-I responses require a positive feedback loop between IRF7 and IFN-I. In recent years, we have discovered that IRF7 is significantly induced and activated by the principal EBV oncoprotein--Latent Membrane Protein 1 (LMP1); however, IRF7 fails to trigger robust IFN-I responses in EBV latency. We believe

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28

zhang, qifang. "Role of Jak/Stat pathway in the pathogenesis of breast cancer." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/41.

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The Jak/Stat signaling cascade mediates cell proliferation, differentiation, survival, apoptosis and immune responses. Aberrant activation of this pathway mediates neoplastic transformation and abnormal growth of many malignancies including breast cancer, the most common cancer among women, and the second leading cause of cancer deaths in women in United States. The mechanism by which the Jak/Stat pathway modulates the pathogenesis of breast cancer is unclear. This dissertation elucidates roles of Jak/Stat members that mediate the pathogenesis of breast cancer. For these studies, we used 4T1

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29

Murtfeldt, Eric Robert. "Consequences of ectopic JAK/STAT pathway activation in the Drosophila male germline." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1457319.

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Thesis (M.S.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed November 5, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 51).

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30

Tardif, Nicolas. "Mechanosignaling through Caveolae : A New Role for the Control of JAK-STAT Signaling." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS337/document.

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Les cavéoles sont des invaginations en forme de coupelle à la membrane plasmique. Ces organelles multifonctionnelles jouent entre autres, un rôle clé dans la mécano-protection et la signalisation cellulaire. En effet, les cavéoles ont la faculté de s’aplanir en réponse à l’augmentation de la tension membranaire, afin de protéger la cellule des contraintes mécaniques. Les cavéoles jouant un rôle clé dans la signalisation cellulaire, nous avions émis l’hypothèse que le cycle mécano-dépendent de désassemblage/réassemblage des cavéoles constitue un interrupteur mécanique de certaines voies de sign

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31

Shen, Ying. "The JAK/STAT pathway in Drosophila hematopoiesis: function and regulatory mechanisms." Ohio : Ohio University, 2007. http://www.ohiolink.edu/etd/view.cgi?ohiou1194628059.

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32

Matlock, Jennifer Renee. "THE JAK-STAT PATHWAY IS REQUIRED FOR MULTIPLE EARLY EVENTS IN DROSOPHILA OOGENESIS." UKnowledge, 2002. http://uknowledge.uky.edu/gradschool_theses/205.

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The Janus kinase (JAK) pathway is an integral part of signaling through a variety of ligands and receptors in mammals. The extensive reutilization and pleiotropy of this pathway in vertebrate development is conserved in other animals as well. In Drosophila melanogaster, JAK signaling is involved in embryonic pattern formation, sex determination, larval blood cell development, wing venation, planar polarity in the eye, and formation of other adult structures. Here we describe several roles for JAK signaling in Drosophila oogenesis. The gene for a JAK pathway ligand, unpaired, is expressed speci

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33

Strickland, Janae. "The Role of STAT and the Jak/STAT Pathway In Mediating the Effects of Interleukin-6 on StAR Expression." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd1781.pdf.

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34

Xi, Rongwen. "Roles of the JAK pathway in follicular patterning of drosophila." Lexington, Ky. : [University of Kentucky Libraries], 2002. http://lib.uky.edu/ETD/ukybiol2002d00063/ThesisRX.pdf.

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Thesis (Ph. D.)--University of Kentucky, 2002.<br>Title from document title page. Document formatted into pages; contains vii, 83 p. : ill. Includes abstract. Includes bibliographical references (p. 73-82).

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35

Paliouras, Grigorios Nikiforos. "Effect of ethanol on the Jak-Stat pathway : is this an NMDA mediated event?" Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79062.

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Alcohol affects many neurochemical processes, causing long-lasting changes in both the adult and developing brain. The Jak-Stat transcriptional activation pathway plays a role in the control of neuronal proliferation, survival and differentiation, but the effects of ethanol on the system have not been fully elucidated. The goal of this project was to define the effects of acute and subchronic ethanol exposure on the expression of proteins in the Jak-Stat pathway, using cultured NG108-15 cells, and in addition, to test the hypothesis that these effects are mediated through the NMDA recep

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36

Etter, Jonathan Parker. "Development of Inhibitors in the IL-6/GP130/JAK/STAT Pathway as Therapeutic Agents." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376525461.

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37

Talerico, Cassandra. "Temporal Activation of the JAK-STAT Pathway in Relation to Cardiac Gene Expression in a Mouse Model of Cardiac Dysfunction." Cleveland State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=csu1197055735.

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38

Fagan, Erin A. "Identification of the presence and activity of the JAK-STAT pathway in canine solid tumors." Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/100859.

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Background: The JAK-STAT pathway is a cellular signaling pathway, which acts normally in humans and animals in the control of multiple important functions. Dysregulation of this pathway has been identified in human cancers, as well as a limited number of veterinary cancers. Objectives: The aims of this study were to identify the presence and tentative activity of components of the JAK-STAT pathway in selected canine tumors. Methods: Formalin-fixed, paraffin-embedded samples from mast cell tumors (MCT), hemangiosarcomas (HSA), thyroid carcinomas, and apocrine gland anal sac adenocarcinomas (AGA

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Silver, Debra L. "A novel role for JAK/STAT signaling in cell migration during development and in cancer." Available to US Hopkins community, 2003. http://wwwlib.umi.com/dissertations/dlnow/308076.

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40

Wells, R. E. "The roles of the JAK/STAT pathway and Fasciclin III in epithelial structures during Drosophila development." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/2658/.

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The processes which drive morphogenesis during Drosophila development are well studied. However, the mechanisms employed to preserve the structures formed as a result of these events are poorly understood. The work of this thesis examines the role of localised cell signalling in effecting the morphogenesis of epithelial tissues. The Drosophila embryonic hindgut is a curved epithelial tube which undergoes elongation and rotation to form a shepherd's crook shaped organ which breaks with the symmetry of the embryo. Work within this thesis describes how asymmetric JAK/STAT signalling, on the insid

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Lee, Eunjoo Hwang. "Effects of Ehrlichia chaffeensis infection on cytokine gene expression and Jak/Stat signaling in human monocytes /." The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487943341528204.

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42

Rush, Craig Michael. "Crosstalk between the Jak-Stat and Wingless pathways is mediated by Mad in Drosophila melanogaster larval hematopoiesis." Ohio University Art and Sciences Honors Theses / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ouashonors1367508013.

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43

Ruez, Richard. "Mécanotransduction par les cavéoles : rôle dans l'activation de stat3 par l'interferon alpha." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA112232.

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Hypothèse : Notre équipe étudie le rôle, mal connu, du trafic membranaire dans le contrôle de l’activation de la voie de signalisation JAK/STAT par les interférons (IFN), une voie clé du contrôle des processus cancéreux. La liaison de l’IFN-a à son récepteur IFNAR active les kinases JAK1 et TYK2 puis des transducteurs de signal comme STAT1, antiprolifératif, ou STAT3, qui a un pouvoir oncogénique. Le laboratoire a démontré récemment que le trafic membranaire d’IFNAR détermine la spécificité du signal des différents IFNs.L’objet de cette thèse est l’étude du rôle des cavéoles dans ce contrôle.

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Denley, Simon M. "The role of the systemic inflammatory response, the JAK STAT pathway and the MAPK pathway in the prognosis of resectable pancreatic cancer." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/523/.

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Pancreatic cancer is a devastating disease with a five year survival of only 2-3%. Only 10-15% of patients have resectable disease at presentation and the only potential cure is major surgery with adjuvant chemotherapy. The outcomes of surgery are disappointing with a median survival of only15-17 months and operative mortality and morbidity figures of 5-10% and 40% respectively. This abysmal prognosis is likely due to the highly aggressive nature of the tumour, its resistance to adjuvant therapy, its late presentation and the likely presence of micro-metastases not detectable at staging or sur

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Lo, Amanda Susana. "Role of Genes in the Jak-Stat Pathway in the Innate Immune System and Immunosenescence in Drosophila melanogaster." Thesis, University of Maryland, Baltimore County, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10275514.

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<p> For many organisms, the immune system tends to deteriorate with age, leading to higher susceptibility to foreign pathogens. While several biological pathways are associated with immunity, the components of the Janus-kinase-Signal Transducers and Activators of Transcription (JAK-STAT) pathway on immunity at different age groups is unclear. This study explored the knock down effects of the <i>Drosophila</i> JAK-STAT pathway components and a candidate gene, <i>robo3,</i> in blood cells. Assessments of immune function were conducted through bacterial clearance assays and phagocytosis assay at

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46

Sun, Yanyong [Verfasser]. "Role of JAK-STAT signaling in the pathogenesis of astrogliosis in chronic demyelinating Theiler’s murine encephalomyelitis / Yanyong Sun." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2013. http://d-nb.info/1046851020/34.

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You, Jia. "Functions of Heparan Sulfate Proteoglycans in Cell Signaling and Stem Cell Regulation during Drosophila Development." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1383644902.

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Chang, Samantha J. "p53, CLIC, AND THE JAK/STAT PATHWAY: INVESTIGATING THE LINK BETWEEN CANCER STRESSES AND CELL DEATH IN DROSOPHILA MELANOGASTER." Ohio University Honors Tutorial College / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1399820564.

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Powers, Nathan Anthony. "Involvement of JAK/STAT Signaling and a Basement Membrane-Associated Protein during Air Sac Primordium Development in Drosophila Melanogaster." TopSCHOLAR®, 2018. https://digitalcommons.wku.edu/theses/3089.

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Abstract:

Tumor metastasis currently presents the greatest obstacle for effective cancer remediation. Metastatic growth necessitates both degradation of a specialized form of extracellular matrix (ECM) known as the basement membrane (BM) and the invasion of surrounding tissues thereafter. The thoracic air sacs of fruit flies (Drosophila melanogaster), which develop and operate in a fashion comparable to the human lung, provide a unique model for identifying and characterizing factors that contribute to its own development as well as tumoral invasion. We investigated the involvement of both Janus kinase

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Chakraborty, Rikhia. "Homeostatic Regulation of Interleukin-4-Mediated Cell Signaling." Cleveland State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1258663290.

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