Relevant bibliographies by topics / MYCIN

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'MYCIN'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "MYCIN"

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Sticklen, Jon, B. Chadrasekaran, J. W. Smith, and John Svirbely. "MDX-MYCIN: The MDX paradigm applied to the mycin domain." Computers & Mathematics with Applications 11, no. 5 (May 1985): 527–39. http://dx.doi.org/10.1016/0898-1221(85)90055-0.

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Edelman, Elazer R., Michael Simons, Martin G. Sirois, and Robert D. Rosenberg. "c-mycin Vasculoproliferative Disease." Circulation Research 76, no. 2 (February 1995): 176–82. http://dx.doi.org/10.1161/01.res.76.2.176.

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Ju, Xiaoli, Meijia Ren, Keping Chen, and Qiang Wang. "Overexpression of c-Myc enhances recombinant protein production in High Five cells after baculovirus infection." Zeitschrift für Naturforschung C 73, no. 3-4 (February 23, 2018): 147–51. http://dx.doi.org/10.1515/znc-2017-0076.

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AbstractDue to their numerous advantages, baculovirus expression vector systems (BEVS) have been widely used to express recombinant proteins for different purposes. Different strategies have been adopted to increase recombinant protein production. In this study, we transiently or stably expressed mousec-Mycin High Five cells using a commercial pIB/V5 vector. Under the control of theOpIE2promoter, this vector could enhance recombinant protein production. We found that transient expression ofc-Mycin High Five cells improved recombinant protein production. Furthermore, we established two stable cell lines, High Five-c-Myc #1 and High Five-c-Myc #2, that stably expressed mousec-Myc. We further found that the expression level of the recombinant protein was increased in these stable cell lines compared to control cell lines. These data indicate that overexpressingc-Mycin cells is a promising way to improve recombinant protein production in BEVS.
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Hirvonen, Harri, Veijo Hukkanen, Toivo T. Salmi, Tarja-Terttu Pelliniemi, and Riitta Alitalo. "L-mycand N-mycin Hematopoietic Malignancies." Leukemia & Lymphoma 11, no. 3-4 (January 1993): 197–205. http://dx.doi.org/10.3109/10428199309086996.

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Daniel, Milan, Petr Hájek, and Phuong Hoang Nguyen. "CADIAG-2 and MYCIN-like systems." Artificial Intelligence in Medicine 9, no. 3 (March 1997): 241–59. http://dx.doi.org/10.1016/s0933-3657(96)00376-4.

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Wallace, Stephanie J., Jian Li, Craig R. Rayner, Kingsley Coulthard, and Roger L. Nation. "Stability of Colistin Methanesulfonate in Pharmaceutical Products and Solutions for Administration to Patients." Antimicrobial Agents and Chemotherapy 52, no. 9 (July 7, 2008): 3047–51. http://dx.doi.org/10.1128/aac.00103-08.

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ABSTRACT Colistin methanesulfonate (CMS) has the potential to hydrolyze in aqueous solution to liberate colistin, its microbiologically active and more toxic parent compound. While conversion of CMS to colistin in vivo is important for bactericidal activity, liberation of colistin during storage and/or use of pharmaceutical formulations may potentiate the toxicity of CMS. To date, there has been no information available regarding the stability of CMS in pharmaceutical preparations. Two commercial CMS formulations were investigated for stability with respect to colistin content, which was measured by a specific high-performance liquid chromatography method. Coly-Mycin M Parenteral (colistimethate lyophilized powder) was stable (<0.1% of CMS present as colistin) for at least 20 weeks at 4°C and 25°C at 60% relative humidity. When Coly-Mycin M was reconstituted with 2 ml of water to a CMS concentration of 200 mg/ml for injection, Coly-Mycin M was stable (<0.1% colistin formed) for at least 7 days at both 4°C and 25°C. When further diluted to 4 mg/ml in a glucose (5%) or saline (0.9%) infusion solution as directed, CMS hydrolyzed faster at 25°C (<4% colistin formed after 48 h) than at 4°C (0.3% colistin formed). The second formulation, CMS Solution for Inhalation (77.5 mg/ml), was stable at 4°C and 25°C for at least 12 months, as determined based on colistin content (<0.1%). This study demonstrated the concentration- and temperature-dependent hydrolysis of CMS. The information provided by this study has important implications for the formulation and clinical use of CMS products.
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LACAVE, CARMEN, and FRANCISCO J. DIEZ. "A review of explanation methods for heuristic expert systems." Knowledge Engineering Review 19, no. 2 (June 2004): 133–46. http://dx.doi.org/10.1017/s0269888904000190.

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Explanation of reasoning is one of the most important abilities an expert system should provide in order to be widely accepted. In fact, since MYCIN, many expert systems have tried to include some explanation capability. This paper reviews the methods developed to date for explanation in heuristic expert systems.
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Bisso, Andrea, Arianna Sabò, and Bruno Amati. "MYCin Germinal Center‐derived lymphomas: Mechanisms and therapeutic opportunities." Immunological Reviews 288, no. 1 (March 2019): 178–97. http://dx.doi.org/10.1111/imr.12734.

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Narain, S. "Special Feature Mycin: Implementing the Expert System in Loglisp." IEEE Software 2, no. 3 (May 1985): 83–88. http://dx.doi.org/10.1109/ms.1985.231028.

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Kersten, Marie José, and Jeroen E. J. Guikema. "MYCin diffuse large B-cell lymphoma: always the bad guy?" Leukemia & Lymphoma 56, no. 11 (June 18, 2015): 3003–4. http://dx.doi.org/10.3109/10428194.2015.1048445.

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Dissertations / Theses on the topic "MYCIN"

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Roberti, Michele. "Sistemi esperti: Mycin come caso di studio." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amslaurea.unibo.it/8358/.

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I sistemi esperti sono programmi che cercano di riprodurre le prestazioni di esperti umani nella risoluzione di problemi specifici. Essi rappresentano il più conosciuto risultato pratico della ricerca in intelligenza artificiale. Ne vengono analizzate la struttura interna, i paragidmi su cui si basano, i componenti che ne fanno parte e i linguaggi di programmazione principali. Viene studiato uno dei primi distemi esperti: il MYCIN. Esso opera nel campo medico ed è stato di notevole importanza e innovazione nei primi anni in cui questi sistemi venivano sviluppati.
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George, Rani Elizabeth. "Gene co-amplification with MYCN in neuroblastoma." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363879.

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Kenyon, Rebecca Margaret. "Analysis of the MYCN amplicon in neuroblastoma." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321261.

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Stermann, Alexander. "MYCN-DNA-Vakzine zur Behandlung des Neuroblastoms." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://dx.doi.org/10.18452/16888.

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Das Neuroblastom (NB) zählt zu den therapieresistentesten Tumoren des Kleinkindalters. Besonders NB-Patienten mit MYCN-Amplifikation sind mit einer schlechten Prognose konfrontiert. Neuere Studien legen nahe, dass eine spezifische aktive Immuntherapie gegen MYCN ein vielversprechender Ansatz zur Bekämpfung dieser malignen Erkrankung darstellen könnte. Zur Untersuchung dieser Hypothese wurde ein sogenanntes Minigen-Vakzin, welches für drei ausgewählte Epitope aus der MYCN-AS-Sequenz kodiert, generiert. Die Auswahl der Minigen-Epitope erfolgte mit dem MHC-Liganden-Vorhersageprogramm syfpeithi, welches drei starke H2-Kk-Liganden lieferte. Außerdem wurden zwei weitere Vakzine hergestellt: als Negativkontrolle MYCNLow, dessen MYCN-Peptide laut syfpeithi schlechte MHC-Klasse-I-Liganden darstellen und ein cDNA-Vakzin auf Basis der gesamten MYCN-cDNA-Sequenz. Zur Applikation der Vakzine wurden attenuierte Salmonella typhimurium SL7207 verwendet, die eine zusätzliche Stimulierung des mukosalen Immunsystems hervorrufen. Für die Untersuchung der Impfstoffe in vivo wurden zwei neuartige immunkompetente NB-Mausmodelle etabliert. Dazu wurden die syngenen NXS2/C1300 A/J-Mausmodelle soweit modifiziert, dass sie über eine induzierbare MYCN-Expression verfügten. Nach Auswahl und Charakterisierung geeigneter Transfektanten in vitro und in vivo wurde in diesen Modellen die Wirksamkeit der Vakzine untersucht. In diesen Versuchen konnte mit Hilfe der Vakzine das Primärtumorwachstum von NXS2-MYCN in geimpften Tieren signifikant im Vergleich zu Kontrollen reduziert und die Metastasierung durch C1300-MYCN Zellen signifikant verzögert werden. Mit den in-vivo-Versuchen anschließenden Analysen wurde schließlich bewiesen, dass die Immunantwort durch tumorinfiltrierende MYCN-spezifische zytotoxische CD8+ T-Zellen vermittelt wird. Zusammenfassend konnte gezeigt werden, dass eine MYCN-DNA-Vakzinierung erfolgreich zur Behandlungen MYCN-exprimierender NB im Mausmodell eingesetzt werden kann.
High-level expression of MYCN protein caused by amplification of the gene characterizes a malignant phenotype of neuroblastoma (NB). Recent studies suggest that MYCN might be a promising target for immunotherapy. Therefore, we investigated the efficacy of three MYCN-specific DNA vaccines. Two minigene vaccines were generated; each encoded for three selected epitopes of the MYCN protein sequence with the highest, or as a control lowest, predicted affinity to MHC-Class-I Molecules. The third vaccine based on the cDNA of MYCN. Salmonella typhimurium SL7207 were used as oral application vehicle for the vaccines in in vivo experiments to induce an additional stimulation of the immune system. To investigate the immunotherapeutic approach NXS2- and C1300-cells syngeneic to immunocompetent A/J-mice were stably transfected with a tetracycline inducible vector system coding for MYCN. The transfectants were characterized and established in vitro and in vivo. In the MYCN-overexpressing models vaccination with the MYCN-DNA-vaccines resulted in significant reduced primary tumor growth or decelerated metastasis spread. The immune responses in the in vivo experiments followed by orally applied MYCN-DNA vaccines was mediated by tumor infiltrating cytotoxic CD8+ and CD4+ T cells. MYCN specificity of infiltrating lymphocytes was verified by MYCN-specific cytolytic activity and IFN-gamma secretion ex vivo. Finally, we showed that blocking of MHC-class I molecule H2-Kk approbated cytotoxicity mediated by CD8+ T cells, indicating MYCN specificity of the induced immune response. In summary, we showed that a MYCN based DNA vaccination strategy is effective against MYCN-expressing NB in vivo. In light of the description of MYCN-specific T cells in NB patients, the lytic action of autologous T cells on MYCN-expressing cells and the results of this study underline the possible potential of an active immunotherapy against MYCN as an alternative therapeutic approach to treat NB.
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Weber, Axel. "Identifizierung und praktische Anwendung molekularer Marker für eine Verbesserung der Prognosebeurteilung humaner Neuroblastome." Doctoral thesis, Universitätsbibliothek Leipzig, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-86808.

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Die Abschätzung der Prognose für Patienten, insbesondere Kinder mit onkologischen Erkrankungen stellt eine große Herausforderung an die behandelnden Ärzte dar. Vor Beginn einer Therapie werden daher viele Informationen gesammelt, um einen Patienten möglichst gut in eine vordefinierte Risikogruppe stratifizieren und dementsprechend eine mehr oder weniger intensive Therapie anbieten zu können. Diese Einteilungen sind allerdings für keinen Malignomtyp mit 100%-iger Sicherheit möglich. Das ist die Ursache dafür, dass auch in niedrige Risikogruppen eingeteilte Patienten nicht auf die Therapie ansprechen und einen unvorhergesehen schlechten Verlauf zeigen können. Auf der anderen Seite scheint es Patienten zu geben, die trotz initial schlecht eingeschätzter Prognose einen überaschend guten Verlauf nehmen, auf die Therapie gut ansprechen und letztlich geheilt werden können. Einen Beitrag zu leisten, um die Stratifizierung für Kinder, die an einem Neuroblastom erkrankt sind, zu verbessern und damit zu vermeiden, dass einige Patienten unter- oder andere Patienten übertherapiert werden müssen, ist das Ziel dieser Habilitationsarbeit. Zu diesem Zweck wurden differentielle, molekulare Marker in primären humanen Neuroblastomen identifiziert und deren prognostische Bedeutung dargestellt. Einzelne dieser Marker (differentiell expremierte mRNAs) wurden in Zellkultursystemen funktionell untersucht, um deren zellbiologische Funktion, die der jeweiligen prognostischen Bedeutung zugrunde liegen kann zu erklären. Desweiteren konnten genomische Merkmale des amplifizierten genomischen Abschnittes auf Chromosom 2p25 um MYCN beschrieben werden. Darauf basierend konnte eine patientenindividuelle und tumorzellspezifische PCR entwickelt werden (AFS-PCR), die sich als Marker für den Nachweis einer minimalen Resterkrankung eignet.
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Maeshima, Ruhina. "MYCN silencing as therapeutics for neuroblastoma using RNA interference." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10043849/.

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Neuroblastoma (NB) is the most common solid tumour in childhood and accounts for 15% of childhood cancer deaths. It is known that high-risk NB is highly correlated with MYCN amplification. Overexpressed MYCN induces proliferation and cell growth and suppresses apoptosis and differentiation pathways in NB cells. Since RNA interference (RNAi) was first described, many research groups have investigated the application of RNAi with the use of short interfering RNA (siRNA). Our aim is to induce apoptosis and differentiation using RNAi as a novel therapeutic strategy for MYCN-amplified NB. Our hypothesis is that MYCN silencing by anti-MYCN siRNA induces apoptosis and differentiation at the mRNA and protein level. We are encapsulating siRNA with liposome and integrin-receptor targeting peptide to deliver MYCN siRNA into NB cells and optimising cationic and anionic polyethylene glycol (PEG)ylated receptor-targeting nanocomplexes (RTNs). In this project, we also aimed to optimise the methods to store RTNs for a long time in trehalose, which is known as a cryoprotectant. As a result, MYCN was silenced by the siRNA at both the mRNA and protein levels, and the siRNA-mediated MYCN reduction induced downstream effects, such as a neuronal differentiation marker TrkA upregulation and the morphological changes of the cells. The anti-MYCN siRNA delivered using RTNs successfully silenced MYCN mRNA in vivo as well. We used an NB cell line with non-functional p53 and resistance toward p53-pathway dependent anti-cancer drugs, probably induced by multiple sessions of chemotherapy and radiotherapy. Therefore, the results are promising for a novel therapy for relapse NB with MYCN amplification. In addition, we successfully demonstrated that trehalose maintains the biophysical properties and the function of RTNs, consisting of either DNA or siRNA at -80 °C. This allows us to make a large amount of RTN for many experiments, store it for the long term, and transport it to a place far from the laboratory.
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Solari, Valeria. "MYCN-dependent expression of sulfatase-2 regulates neuroblastoma cells." Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/2003528/.

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Neuroblastoma (NBL) is the most common type of cancer diagnosed in the first year of life. It is a complex and heterogeneous disease that arises from the developing sympathetic nervous system. Despite numerous advances and the well-demonstrated role of MYCN in the pathogenesis of neuroblastoma, the mechanisms underlying its oncogenic function are not entirely understood and there is evidence that its function is, in part, dependent on the tumour microenvironment (TME). New and improved therapeutic targets are urgently required for this often lethal tumour. Heparan sulfate proteoglycans (HSPG) play a critical role in the interactions between tumour cells and the TME and their activities are dependent on the sulfation pattern, that is controlled by sulfotransferases, which add sulfate groups to the repeating disaccharide units, and sulfatases (SULFs), which selectively remove 6-O-sulfates. In this work an analysis of the expression of these enzymes in human neuroblastoma revealed higher levels of SULF2 specifically when the MYCN oncogene was amplified. Loss of expression of SULF2 in MYCN-amplified (A) cell lines was associated with a marked decrease in survival and an increase in apoptosis. Evidence is presented that SULF2 is a direct downstream target of MYCN since overexpression of MYCN in neuroblastoma cells increases SULF2 expression whereas a down regulation reduced SULF2 expression. Underlying the importance of SULF2 in neuroblastoma cell survival independently of MYCN, it is demonstrated that overexpression of SULF2 in MYCN-NA cells increases cell viability without increasing MYCN expression. Analysis of SULF2 protein expression in a large cohort of primary human neuroblastoma tumours also indicated a high level of expression in MYCN-A tumours and an almost complete absence of expression in MYCN-non A (NA) tumours. The data identify SULF2 as a new downstream target of MYCN and a key contributor to its oncogenic function in human neuroblastoma, which might have future implications for clinical therapies for high-risk NBL.
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Schulze, Franziska. "Die Telomerlänge als Prognosefaktor in MYCN nicht-amplifizierten Neuroblastomen." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-200943.

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Eines der charakteristischen Merkmale des Neuroblastoms stellt seine einzigartige biologische Heterogenität dar, die eine genaue Ausage des weiteren klinischen Verlaufes stark erschwert. Bestimmte prognostisch wirksame klinische, molekularbiologische und genetische Faktoren, wie zum Beispiel Alter bei Erstdiagnose, Tumorstadium, MYCN-Amplifikation und 1p Deletion, werden seit längerem zur Risikostratifizierung genutzt. Bereits in anderen Tumorerkrankungen konnte nun der Einfluß einer Telomerlängenveränderung auf das Gesamtüberleben von Patienten nachgewiesen werden. Telomere sichern die genomische Integrität und bestimmen maßgeblich die proliferative Kapazität jeder somatischen Zelle. Aktuelle Forschungsergebnisse legen die Vermutung nahe, dass Veränderungen der Telomerlänge auch in Neuroblastomen einen prognostischen Effekt auf das Gesamtüberleben haben. In diesem Kontext untersucht die vorliegende Arbeit den Zusammenhang zwischen Telomerlänge und Gesamtüberleben in 420 MYCN nicht-amplifizierten primären Neuroblastomen mit Erstdiagnosen von 1983-2001. Hierfür wurden die relativen Telomerlängen mithilfe einer neu etablierten monochromen multiplex q-RT-PCR ermittelt. Anschließend wurden diese sowohl mit ausgesuchten klinischen Variablen (Alter bei Erstdiagnose, Tumorstadium, Primärlokalisation des Tumors, Histologie, Geschlecht und Rezidivauftreten) korreliert als auch auf ihren Einfluß auf das Gesamt- und ereignisfreie Überleben untersucht. In Korrelation mit den klinischen Parametern konnte zwischen Alter bei Erstdiagnose und Telomerlänge ein eindeutiger Zusammenhang nachgewiesen werden. Je älter die Patienten bei Erstdiagnose, desto höher war sowohl der Anteil verlängerter Telomere als auch der extremer Telomerlängenveränderungen. Neuroblastome mit verlängerten Telomeren zeigten in der gleichen Altersgruppe ein verringertes Gesamtüberleben der betroffenen Patienten verglichen mit Neuroblastomen mit verkürzten Telomeren. Somit könnte eine Telomerlängenveränderung, insbesondere verlängerte Telomere, im klinischen Alltag als Hinweis auf einen prognostisch ungünstigen Verlauf genutzt werden.
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Valli, Emanuele <1983&gt. "The role of MYCN-mediated transcriptional repression in neuronal physiopathology." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4809/.

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MYC is a transcription factor that can activate transcription of several targets by direct binding to their promoters at specific DNA sequences (E-box). Recent findings have also shown that it can exert its biological role by repressing transcription of other set of genes. C-MYC can mediate repression on its target genes through interaction with factors bound to promoter regions but not through direct recognition of typical E-Boxes. In this thesis, we investigated whether MYCN can also repress gene transcription and how this is mechanistically achieved. Moreover, expression of TRKA, P75NTR and ABCC3 is attenuated in aggressive MYCN-amplified tumors, suggesting a causal link between elevated MYCN activity and transcriptional repression of these three genes. We found that MYCN is physically associated with gene promoters in vivo in proximity of the transcriptional start sites and this association requires interactions with SP1 and/or MIZ-1. Furthermore, we show that this interaction could interfere with SP1 and MIZ-1 activation functions by recruiting co-repressors such as DNMT3a or HDACs. Studies in vitro suggest that MYCN interacts through distinct domains with SP1, MIZ-1 and HDAC1 supporting the idea that MYCN may form different complexes by interacting with different proteins. Re-expression of endogenous TRKA and P75NTR with exposure to the TSA sensitizes neuroblastoma to NGF-mediated apoptosis, whereas ectopic expression of ABCC3 decreases cell motility without interfering with growth. Finally, using shRNA whole genome library, we dissected the P75NTR repression trying to identify novel factors inside and/or outside MYCN complex for future therapeutic approaches. Overall, our results support a model in which MYCN can repress gene transcription by direct interaction with SP1 and/or MIZ-1, and provide further lines of evidence on the importance of transcriptional repression induced by Myc in tumor biology.
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Vulcani-Freitas, Tânia Maria [UNIFESP]. "Perfil de expressão dos genes MYC, MYCN, TERT, ASPM e PRAME em Meduloblastoma." Universidade Federal de São Paulo (UNIFESP), 2010. http://repositorio.unifesp.br/handle/11600/9928.

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Meduloblastoma (MB) é o tumor maligno de sistema nervoso central (SNC) mais comum em criança, compreendendo 20% dos tumores primários de SNC e 40% dos tumores cerebelares da infância. Devido sua forte tendência metastática, o tratamento padrão pós-operatório inclui radio e quimioterapia, cujo impacto causa distúrbios endócrinos e de crescimento, e disfunção neurocognitiva a longo prazo. Frente a esses efeitos negativos, muitas pesquisas em meduloblastoma têm sido realizadas com intuito de obter conhecimento biológico desses tumores para tentar identificar fatores prognósticos moleculares que possam orientar os tratamentos, tornando-os mais específicos e menos agressivos. Alguns estudos em MB têm sugerido que a expressão do oncogene MYC está associada com diminuição da sobrevida e sua superexpressão com maior agressividade do tumor. Por isso, MYC pode ser um indicador importante de prognóstico, além de modulador do comportamento desta doença. Enquanto o gene MYC é expresso em uma variedade de tecidos, a expressão de MYCN, outro membro da família MYC, é restrita a estágios precoces do desenvolvimento embrionário de alguns tecidos apenas, entre eles, o sistema nervoso central e periférico, sendo um mediador importante dos efeitos de ativação na proliferação de células precursoras cerebelares. Dessa forma, quando a expressão de MYCN está desregulada, ela aumenta a tumorigenicidade dessas células podendo dar origem ao MB. Além disso, o gene MYC também é considerado importante regulador da transcrição TERT, gene que codifica uma subunidade catálica de da telomerase, enzima importante para carcinogênese e imortalização de células neoplásicas. A atividade anormal da telomerase está presente em 90% dos cânceres e o aumento de sua atividade está associado a eventos clínicos desfavoráveis. Outro gene importante é o ASPM (abnormal spindle-like microcephaly associated) que desempenha função fundamental na neurogênese e proliferação celular durante o desenvolvimento cerebral. Esse gene codifica uma proteína de centrossomo e fuso mitótico que permite a divisão celular simétrica em células neuroepiteliais durante o desenvolvimento e aumento do tamanho cerebral. Alterações em ASPM é a causa mais comum de microcefalia primária em humanos e de falha de segregação, induzindo a aneuploidias e instabilidade genética. Além desses genes, outro gene estudado recentemente, como alvo em xv imunoterapia, é o gene PRAME que codifica um antígeno tumoral que está presente em vários tumores, incluindo meduloblastoma. O gene PRAME possui baixa ou ausência de expressão em tecidos normais, por isso é pode ser um forte candidato como alvo em imunoterapia, que é um tratamento menos tóxico. OBJETIVOS: O objetivo desse estudo foi investigar a expressão dos genes MYC, MYCN, TERT, ASPM e PRAME em fragmentos tumorais de meduloblastoma de crianças e tentar correlacionar com os parâmetros clínicos e verificar se há correlação de MYC, MYCN, TERT entre si, uma vez que estão correlacionados. MÉTODOS: Análise de expressão gênica foi realizada através de PCR quantitativa em tempo real, utilizando sistema SYBR Green, em 37 amostras tumorais de crianças, com média de idade de 8 anos. Para comparação de perfil de expressão foi usada duas amostra de cérebro normal. A análise estatística foi realizada nos programas Graph Pad Prism 4 e VassarStats RESULTADOS: Todas nossas amostras superexpressaram o gene MYCN com valor de quantificação relativa (RQ) mediana igual a 31 com p=0.001; assim como, todas nossas amostras também superexpressaram o gene ASPM com mediana igual a 586, p<0.0001. Do total de amostras, 95%, 81% e 84% superexpressaram TERT, MYC e PRAME respectivamente, sendo os valores de RQ (mediana) iguais a 322, p=0.01; 9.2, p<0.0001; 33, p<0.0001. Apesar da elevada expressão dos genes estudados na maioria das amostras estudadas, houve apenas correlação estatística entre a superexpressão de MYCN (p=0.008) e os pacientes que foram a óbito, e de TERT e os pacientes que recidivaram (p=0.0431). Não encontramos outra correlação estatística entre a superexpressão dos genes e as características clínicas dos pacientes. CONCLUSÃO: Os genes MYC, MYCN e TERT estavam superexpressos nas amostras de meduloblastoma analisadas em uma freqüência muito superior ao demonstrado na literatura, o que sugere que esses três genes podem ajudar na identificação de tumores agressivos, uma vez que o pognóstico desses pacientes continua baseado apenas em parâmentros clínicos. A superexpressão de ASPM em todas as amostras estudadas sugere que este gene pode estar envolvido na origem de MB, como parte da neurogênse anormal durante o desenvolvimento embrionário, porém estudoas funcionais devem ser realizados para confirmar essa hipótese. Por fim, o gene PRAME pode ser candidato à marcador de célula tumoral em MB, podendo no futuro ser candidato como alvo em imunoterapias.
To investigate the expression of genes MYC, MYCN and TERT in tumor fragments of pediatric medulloblastoma and correlate gene expression profiles with clinical parameters. Analysis of gene expression was performed by quantitative PCR real time in 37 tumor samples and correlated with clinical and pathological data. All 37 samples overexpressed MYCN gene (p= 0.001), 95% and 84% of the samples overexpressed TERT and MYC, respectively (p<0.0001). Twenty nine (78%) of all samples had concomitant high expression of MYC, MYCN and TERT genes together. Seventeen (59%) were high-risk classification, 10 (34%) were metastatic (M+) stage, two (7%) were anaplastic or largecell/ anaplastic subtype, eight (28%) of patients relapsed, beyond thirteen (45%) suffered partial surgical resection. and fourteen (48%) died. We found correlation between MYC, MYCN and TERT expression (p<0.0001). The identification of a subgroup with concomitant overexpression of the three investigated genes suggests the possibility of using more than one aspect of molecular indicative of unfavorable prognosis that characterizes the group with poor outcome. However, in future this may be enhanced by targeted therapy for the product TERT as proposed in some neoplasms. The identification of molecular events in the medulloblastoma categorization aims to help at-risk groups moving towards individualized medicine.
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Books on the topic "MYCIN"

1

Shank, J. Clayton. Mylin ancestry and descendants of Abraham and Elizabeth Myer Mylin. Quarryville, PA (R.D. 4, Box 545, Quarryville 17566): J.C. Shank, 1986.

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Mydin: The untold story. Petaling Jaya, Selangor, Malaysia: MPH Pub., 2012.

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Clancey, William J. Knowledge-based tutoring: The GUIDON program. Cambridge, Mass: MIT Press, 1987.

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Rundle, David F. The Bloodied Lambskin: A Bernie Mylin Murder Mystery. PublishAmerica, 2006.

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Tune Up: The Secrets of Mylin - Book I. Cartosi LLC, 2017.

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Burn Up: The Secrets of Mylin - Book II. Cartosi LLC, 2018.

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Book chapters on the topic "MYCIN"

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Schnupp, Peter, and Ute Leibrandt. "Mycin." In Expertensysteme, 21–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-662-00752-5_3.

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Schnupp, Peter, and Ute Leibrandt. "Mycin." In Expertensysteme, 21–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-95565-5_3.

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Hájek, P. "Towards a Probabilistic Analysis of MYCIN-like Expert Systems (Working Paper)." In Compstat, 117–21. Heidelberg: Physica-Verlag HD, 1988. http://dx.doi.org/10.1007/978-3-642-46900-8_14.

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Kamijo, Takehiko. "Neuroblastoma: Role of MYCN/Bmi1 Pathway in Neuroblastoma." In Pediatric Cancer, 161–67. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2418-1_15.

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Humphries, E. H., and E. J. Filardo. "The Transforming Activity of PP59C-MYCis Weaker Than That of v-myc." In Current Topics in Microbiology and Immunology, 259–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75889-8_32.

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Hatzi, Elissavet, Theodore Fotsis, Carol Murphy, Stephen Breit, Lothar Schweigerer, Andreas Zoephel, Ulrike Tontsch, Horst Ahorn, and Keith Ashman. "MYCN Oncogene and Angiogenesis: Down-Regulation of Endothelial Growth Inhibitors in Human Neuroblastoma Cells." In Advances in Experimental Medicine and Biology, 239–48. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4221-6_19.

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Surace, Cecilia. "Medulloblastoma: Role of MYCN Gene Amplification Using Fluorescence In Situ Hybridization and Real Time Quantitative PCR Methods." In Pediatric Cancer, Volume 3, 137–44. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4528-5_15.

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Yagyu, Shigeki, and Tomoko Iehara. "MYCN Nonamplified Neuroblastoma: Detection of Tumor-Derived Cell-Free DNA in Serum for Predicting Prognosis of Neuroblastoma." In Pediatric Cancer, Volume 4, 11–17. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6591-7_2.

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"COLY-MYCIN (Colistimethate Sodium)." In Antibiotics Manual, 96–97. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119220787.ch43.

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"COLY-MYCIN® M PARENTERAL (Colistimethate for Injection)." In Antibiotics Manual, 94–95. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119220787.ch42.

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Conference papers on the topic "MYCIN"

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O'Callaghan, Thomas A., James Popple, and Eric McCreath. "SHYSTER-MYCIN." In the 9th international conference. New York, New York, USA: ACM Press, 2003. http://dx.doi.org/10.1145/1047788.1047814.

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Zhang, Xiaoju, Shijie Li, and Jiangrong Xiao. "Screening and Fermentation of Jinggang-mycin High-yielding Strains." In 2018 7th International Conference on Energy and Environmental Protection (ICEEP 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/iceep-18.2018.90.

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Chen WenBin, Liu XiaoLing, Liu YiJun, and Fang Yu. "A machine learning algorithm for expert system based on MYCIN model." In 2010 2nd International Conference on Computer Engineering and Technology. IEEE, 2010. http://dx.doi.org/10.1109/iccet.2010.5485424.

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Neapolitan, Richard E. "A Comparison Of The Mycin Model For Reasoning Under Uncertainty To A Probability Based Model." In 1986 Technical Symposium Southeast, edited by John F. Gilmore. SPIE, 1986. http://dx.doi.org/10.1117/12.964152.

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Kuo, Be-Sheng, Gil Korner, and Thorir D. Bjornsson. "ROLE OF POLYAMINES IN THE REGULATION OF SYNTHESIS AND SECRETION OF PLASMINOGEN ACTIVATOR FROM BOVINE AORTIC ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644655.

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Abstract:
The effects of three polyamines, putrescine (PUT), spermidine (SPD) and spermine (SPM), were investigated on the synthesis and secretion of plasminogen activator (PA) and antiactivator (PAI) activities in confluent bovine aortic endothelial cells. PA activity was determined bythe fibrin plate method, and individual species with PA and PAI activities were separated and visualized using SDS-PAGE with zymography and reverse fibrin autography. Both control cells and cells treated with polyamines secreted PA activity in a time-dependent fashion. After 24-hour incubation, the three polyamines enhanced PA secretion in a dose-dependent manner (10-6 to 2.5 × 10-3 M), with a potency order of SPM > SPD> PUT, as estimated by the fibrin plate method. The maximum PA releases after PUT (0.5 mM), SPD (2.5 mM) and SPM (0.5 mM) were 1.7, 4.5 and 5.4 times control levels, respectively. Concentrations lower than 1 μM had essentially no effects. The enhancement of PA activity by polyamines was blocked by actino-mycin D and cycloheximide, while it was not affected by inhibitors of polyamine biosynthesis except that the enhancement by PUT (0.5 mM) was reduced by methylglyoxal bis(guanylhydrazone). These data suggest that polyamines directly stimulate PA synthesis and secretion through promotion of gene transcription and translation, and that this effect appears to be related to their position in the biosynthetic pathway of polyamines. The kinetic patterns of activities of ornithine decarboxylase and S-adenosy-methionine decarboxylase in confluent endothelial cells stimulated withfresh culture medium suggest that there is rapid turnover of intracellular polyamines. Multiple forms of secreted PA were observed and both tissue- and urokinase-type PA were enhanced by polyamines, while the PAI activity, as evaluted by reverse fibrin autograpy, was apparently reduced. These experimental results suggest that polyamines may play an important role in the regulation of the synthesis and secretion of plasminogen activators, and that this biological function could be modified by disease states and by agents that are associated with altered polyamine metabolism.
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Stermann, Alexander, Nicole Huebener, Diana Seidel, Anastasia Shibina, Stefan Fest, Gerhard Gaedicke, and Holger N. Lode. "Abstract 4758: A new syngeneic MYCN-overexpressing neuroblastoma mouse model and MYCN-DNA vaccine." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4758.

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Stermann, Alexander, Nicole Huebener, and Holger N. Lode. "Abstract LB-155: A new syngeneic MYCN-overexpressing neuroblastoma mouse model and MYCN-DNA vaccine." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-155.

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Tanimoto, Terutaka, Hiroshi Tazawa, Hiroshi Noso, Takanori Oyama, Yasuo Urata, Shunsuke Kagawa, Takuo Noda, and Toshiyoshi Fujiwara. "Abstract 5816: Ablation of oncogenic MYCN expression by hTERT-driven oncolytic adenovirus induces cell death in MYCN-amplified neuroblastoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5816.

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Helmsauer, K., M. Valieva, S. Ali, R. Chamorro Gonzalez, R. Schöpflin, JH Schulte, S. Mundlos, RP Koche, and AG Henssen. "Enhancer hijacking on the MYCN amplicon in neuroblastoma." In 33. Jahrestagung der Kind-Philipp-Stiftung für pädiatr. onkolog. Forschung. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1709775.

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Trajkovski, Marko, Metka Vivod, Mateus Webba da Silva, and Janez Plavec. "G-Quadruplex formation within proximal promoter of MYCN." In XVth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201112483.

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Reports on the topic "MYCIN"

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George, Rani E. A Genetically Engineered Mouse Model of Neuroblastoma Driven by Mutated ALK and MYCN. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613947.

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