Relevant bibliographies by topics / Tumor necrosis factor

Contents

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

Academic literature on the topic 'Tumor necrosis factor'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 June 2025

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Journal articles on the topic "Tumor necrosis factor"

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KEYSTONE, E. C., and C. F. WARE. "Tumor Necrosis Factor and Anti-Tumor Necrosis Factor Therapies." Journal of Rheumatology Supplement 85 (May 1, 2010): 27–39. http://dx.doi.org/10.3899/jrheum.091463.

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Chung, Phil-Sang, та Pil-Seob Jeong. "Antitumor effect of Tumor Necrosis Factor-α". Journal of Clinical Otolaryngology Head and Neck Surgery 7, № 1 (травень 1996): 45–55. http://dx.doi.org/10.35420/jcohns.1996.7.1.45.

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Inoue, Mamoru, Hidetoshi Inoko, and Kimiyoshi Tsuji. "Tumor necrosis factor." Ensho 12, no. 1 (1992): 21–32. http://dx.doi.org/10.2492/jsir1981.12.21.

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Old, Lloyd J. "Tumor Necrosis Factor." Scientific American 258, no. 5 (May 1988): 59–75. http://dx.doi.org/10.1038/scientificamerican0588-59.

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Wenzel, Richard P., Roger C. Bone, and Michel P. Glauser. "Tumor necrosis factor." Critical Care Medicine 21, Supplement (October 1993): S414–422. http://dx.doi.org/10.1097/00003246-199310001-00001.

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TRACEY, KEVIN J., and ANTHONY CERAMI. "Tumor necrosis factor." Critical Care Medicine 21, Supplement (October 1993): S423–435. http://dx.doi.org/10.1097/00003246-199310001-00002.

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Vilcek, J., and T. H. Lee. "Tumor necrosis factor." Journal of Biological Chemistry 266, no. 12 (April 1991): 7313–16. http://dx.doi.org/10.1016/s0021-9258(20)89445-9.

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Chu, Wen-Ming. "Tumor necrosis factor." Cancer Letters 328, no. 2 (January 2013): 222–25. http://dx.doi.org/10.1016/j.canlet.2012.10.014.

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Duerrschmid, Clemens, JoAnn Trial, Yanlin Wang, Mark L. Entman, and Sandra B. Haudek. "Tumor Necrosis Factor." Circulation: Heart Failure 8, no. 2 (March 2015): 352–61. http://dx.doi.org/10.1161/circheartfailure.114.001893.

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Varfolomeev, Eugene E., and Avi Ashkenazi. "Tumor Necrosis Factor." Cell 116, no. 4 (February 2004): 491–97. http://dx.doi.org/10.1016/s0092-8674(04)00166-7.

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Dissertations / Theses on the topic "Tumor necrosis factor"

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Björnberg, Flemming. "Processing of TNF-receptors to soluble receptor forms in myeloid cells." Lund : Dept. of Hematology, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39176479.html.

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Engelberts, Ingeborg. "Tumor necrosis factor during sepsis king of cytokines? /." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6955.

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Krugten, Michiel Volkert van. "Tumor necrosis factor gene polymorphisms and rheumatic diseases /." Leiden, 2003. http://catalogue.bnf.fr/ark:/12148/cb40223074h.

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Oukacha, Khadija. "Perturbation chimique du transport de Tumor Necrosis Factor." Electronic Thesis or Diss., Université Paris sciences et lettres, 2023. http://www.theses.fr/2023UPSLS067.

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Alors qu'il est essentiel pour lutter contre les agents pathogènes, TNF (Tumor Necrosis factor) secrété́ en excès devient nocif pour l'organisme comme dans le cas de maladies inflammatoires chroniques (polyarthrite rhumatoïde ou maladie de Crohn). Les thérapies actuelles sont basées sur des injections récurrentes d'anti-TNF contre lesquelles 30% des patients développent une résistance. Il existe donc un fort besoin de composés chimiques réduisant la sécrétion de TNF. Nous avons exploité la diversité́ des voies de sécrétion dépendantes de l’appareil de Golgi pour identifier des molécules inhibant spécifiquement la sécrétion de TNF. L’outil RUSH (Retention Using Selective Hooks) a permis la synchronisation et l’analyse du transport de TNF dans les cellules HeLa. En combinant le test RUSH à un criblage phénotypique différentiel de banques chimiques, 85 molécules inhibant le transport de TNF ont été sélectionnées. Les effets de certaines molécules ont été validés. Seules les molécules inhibantes au moins 40% de la sécrétion de TNF ont été retenues. La spécificité de ces molécules sur le transport d’autres protéines, à savoir EGFP-GPI et IL-6 a été évaluée. Les 14 molécules inhibantes plutôt spécifiquement la sécrétion de TNF ont été retenues pour poursuivre leur caractérisation en modèle physiologique.Les effets des molécules sur la sécrétion endogène de TNF et d’autres cytokines ont été mesurés dans des monocytes et des macrophages primaires humains issus du sang de donneurs après incubation avec du lipopolysaccharide (LPS) bactérien. Ces expériences en modèles physiologiques ont mis en évidence trois molécules capables d'inhiber significativement la sécrétion endogène de TNF sans affecter la sécrétion d'IL-8. Des expériences de dose-réponse et l’évaluation des effets des molécules sur l’expression de TNF ont été réalisées pour aider dans la compréhension du mode d’action de ces molécules.En conclusion, le criblage chimique, les expériences en modèle hétérologue puis en modèles physiologiques ont permis d'identifier 3 molécules inhibant la sécrétion de TNF. Ces résultats confirment que la diversité́ des voies sécrétoires est suffisamment grande pour cibler le transport d'une protéine impliquée dans une maladie et pourraient ouvrir la voie à des traitements alternatifs ou complémentaires contre les maladies inflammatoires<br>While it is essential to fight against pathogens, TNF (Tumor Necrosis factor) secreted in excess becomes harmful to the body as in the case of chronic inflammatory diseases (rheumatoid arthritis or Crohn's disease). Current therapies are based on recurrent injections of anti-TNF against which 30% of patients develop resistance. There is therefore a strong need for chemical compounds which reduce the secretion of TNF. We have exploited the diversity of secretory pathways dependent on the Golgi apparatus to identify molecules that specifically inhibit TNF secretion. The RUSH (Retention Using Selective Hooks) tool allowed the synchronization and analysis of TNF transport in HeLa cells. By combining the RUSH assay with a differential hight content screening of chemical libraries, 85 molecules inhibiting TNF transport were selected. The effects of certain molecules have been validated. Only molecules inhibiting at least 40% of TNF secretion were retained. The specificity of these molecules on the transport of other proteins, namely EGFP-GPI and IL-6 was evaluated. The 14 molecules rather specifically inhibiting the secretion of TNF were selected to continue their characterization in a physiological model.The effects of the molecules on the endogenous secretion of TNF and other cytokines were measured in human primary monocytes and macrophages obtained from blood donors after incubation with bacterial lipopolysaccharide (LPS). These experiments in physiological models have demonstrated three molecules capable of significantly inhibiting the endogenous secretion of TNF without affecting the secretion of IL-8. Dose-response experiments and the evaluation of the effects of molecules on the expression of TNF have been carried out to help in understanding the mode of action of these molecules.In conclusion, the chemical screening, the experiments in heterologous model then in physiological models made it possible to identify 3 molecules inhibiting the secretion of TNF. These results confirm that the diversity of secretory pathways is large enough to target the transport of a protein involved in a disease and could open the way to alternative or complementary treatments against inflammatory diseases
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Watts, Alan D. "The biological role of transmembrane tumour necrosis factor [alpha]." Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27668.

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Tumour necrosis factor (TNF) exists in two physiological forms. One is a soluble polypeptide of 17 kDa, and the other a type II integral membrane protein of 26 kDa designated transmembrane TNF. Soluble TNF is derived from the transmembrane form by proteolytic processing. The soluble TNF molecule exerts potent cytotoxic activity against certain types of cancer cells, and plays a critical role in the functioning of the immune and inflammatory system. The transmembrane TNF molecule shares many of the properties of the soluble form in vitro, but its function in the immune system is not as clearly defined as for the sTNF form. In this thesis the biological role of transmembrane TNF was investigated. The synthesis and expression of both soluble TNF and transmembrane TNF forms was examined in macrophage cells stimulated with LPS. Basic parameters for the production of transmembrane TNF were established to enable further analysis of its function. Using a hydroxamic acid-based inhibitor of TNF processing it was possible to obtain macrophage cells that expressed transmembrane TNF, but not soluble TNF; This enabled the investigation of transmembrane TNF free from the complicating effects of soluble TNF. It was found that inhibition of TNF processing in this way caused an accumulation of transmembrane TNF on the macrophage cells surface 5.1-7.5-fold greater than in cells not treated with the hydroxamic acid-based inhibitor. This corresponded to a 6.4-fold increase in TNF-mediated cytotoxicity of macrophage cells towards cells sensitive to transmembrane TNF. By radiolabelling macrophages, and using a specialised immunoprecipitation method, it was demonstrated that a soluble form of one of the TNF receptors (sTNFFi) binds transmembrane TNF. The consequence of this binding was neutralisation of transmembrane TNF-mediated cytotoxicity, but not inhibition of proteolytic processing of transmembrane TNF to release soluble TNF. The possibility that transmembrane TNF is capable of transducing a signal upon ligation with sTNFR was investigated. A broad range of cellular parameters were measured to see whether sTNFFi treatment of macrophages expressing transmembrane TNF induced a biochemical/physiochemical change. It was found that sTNFR caused a large increase (~200%) in ix intracellular calcium levels after 15 min treatment. This is the first direct evidence that transmembrane TNF is capable of acting like a receptor. The composition of the predicted amino acid sequence of transmembrane TNF was closely examined to determine the presence of features important for both structure and intracellular signalling. A model is presented in Chapter 6 which outlines in diagrammatic form likely structural features of transmembrane TNF. The molecule is predicted to possess a region of cytoplasmic alpha-helices corresponding to a highly conserved domain of the sequence. The structure of transmembrane TNF is consistent with that of a transmembrane receptor, capable of transducing signals initiated by ligation with an extracellular ligand. The comparison of predicted amino acid sequences of transmembrane TNF from different mammalian species revealed the presence of a conserved casein kinase | site. This site was also found to be present in most members of the TNF ligand family. Using orthophosphate labelling, it was shown that mouse transmembrane TNF is phosphorylated in macrophages. Ligation of sTNFR with transmembrane TNF induced de-phosphorylation of mTNF. This de-phosphorylation could be prevented by pre-incubation of the cells with serine phosphatase inhibitors. A selective inhibitor of casein kinase | dramatically reduced the phosphorylation of transmembrane TNF produced by macrophages. In addition, a recombinant form of casein kinase l phosphorylated transmembrane TNF in vitro on the site naturally phosphorylated by the endogenous kinase in vivo. The evidence presented in this study supports an entirely new role for transmembrane TNF, one in which the molecule is capable of acting like a transmembrane receptor, with the ligand being sTNFR. This phenomenon is known as "reverse signalling", and has been shown by other researchers to occur in the majority of members of the TNF ligand family. Implications of mTNF "reverse signalling" are relevant to the treatment of human diseases in which sTNFRs are currently being assessed in clinical trials.
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Langton, Amy Jean. "The role of TRUSS in TNFα-TNFRI signalling : implications for inflammatory lung diseases". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608019.

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Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /." Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.

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Bond, Arden Lenore. "The production and characterization of a putative anti-idiotypic antibody to tumor necrosis factor-[alpha] /." This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-05042010-020132/.

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Tan, Ern Yu. "Loss of protein folding gene expression in human tumors." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670106.

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Han, Jiahuai. "Study of the regulation of cachectin/tumor necrosis factor expression." Doctoral thesis, Universite Libre de Bruxelles, 1990. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213139.

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Books on the topic "Tumor necrosis factor"

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Corti, Angelo, and Pietro Ghezzi. Tumor Necrosis Factor. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592597718.

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National Institutes of Health (U.S.), ed. Tumor necrosis factor. [Bethesda, Md.?: National Institutes of Health, 1989.

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National Institutes of Health (U.S.), ed. Tumor necrosis factor. [Bethesda, Md.?: National Institutes of Health, 1989.

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Sanjay, Khare, ed. TNF superfamily. Austin, Tex: Landes Bioscience, 2007.

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Angelo, Corti, and Ghezzi P, eds. Tumor necrosis factor: Methods and protocols. Totowa, N.J: Humana Press, 2004.

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Sanjay, Khare, ed. TNF superfamily. Austin, Tex: Landes Bioscience, 2007.

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Gregory, Bock, Marsh Joan, and Symposium on Tumour Necrosis Factor and Related Cytotoxins (1987 : London, England), eds. Tumour necrosis factor and related cytotoxins. Chichester: Wiley, 1987.

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F, Oettgen Herbert, and International Cancer Research Data Bank., eds. Selected abstracts on tumor necrosis factor. [Bethesda, M.D.?]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, International Cancer Research Data Bank, National Cancer Institute, 1987.

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Bruce, Beutler, ed. Tumor necrosis factors: The molecules and their emerging role in medicine. New York: Raven Press, 1992.

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Benjamin, Bonavida, ed. Tumor necrosis factor/cachectin and related cytokines. Basel: Karger, 1988.

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Book chapters on the topic "Tumor necrosis factor"

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Chu, Wen-Ming. "Tumor Necrosis Factor." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_6040-8.

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Barger, Steven W. "Tumor Necrosis Factor." In Neuroprotective Signal Transduction, 163–83. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-475-7_9.

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Chu, Wen-Ming. "Tumor Necrosis Factor." In Encyclopedia of Cancer, 4679–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_6040.

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Ulich, Thomas R. "Tumor Necrosis Factor." In Cytokines of the Lung, 307–32. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003066927-11.

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Manogue, Kirk R., and Anthony Cerami. "Cachectin (Tumor Necrosis Factor)." In Cellular and Molecular Aspects of Inflammation, 123–50. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5487-1_8.

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Brightling, Christopher, Latifa Chachi, Dhan Desai, and Yassine Amrani. "Tumor Necrosis Factor Alpha." In Inflammation and Allergy Drug Design, 225–35. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch18.

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Johnson, Victor J. "Tumor Necrosis Factor-α." In Encyclopedia of Immunotoxicology, 927–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_1522.

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Arampatzis, Adamantios, Lida Mademli, Thomas Reilly, Mike I. Lambert, Laurent Bosquet, Jean-Paul Richalet, Thierry Busso, et al. "Tumor Necrosis Factor Alpha." In Encyclopedia of Exercise Medicine in Health and Disease, 883. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3152.

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Papp, K. A., and Mathew N. Nicholas. "Tumor Necrosis Factor Inhibition." In Biologic and Systemic Agents in Dermatology, 111–21. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66884-0_13.

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Johnson, Victor J. "Tumor Necrosis Factor-α." In Encyclopedia of Immunotoxicology, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27786-3_1522-2.

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Conference papers on the topic "Tumor necrosis factor"

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Goel, Raghav, Guilio F. Paciotti, and John C. Bischof. "Tumor necrosis factor-alpha induced enhancement of cryosurgery." In Biomedical Optics (BiOS) 2008, edited by Nikiforos Kollias, Bernard Choi, Haishan Zeng, Reza S. Malek, Brian J. Wong, Justus F. R. Ilgner, Kenton W. Gregory, Guillermo J. Tearney, Henry Hirschberg, and Steen J. Madsen. SPIE, 2008. http://dx.doi.org/10.1117/12.764020.

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Blanco, A., R. Bonfil, O. Bustoabad, and M. Lazzari. "FACTOR II ACTIVATING ACTIVITY IN EXTRACTS OF TUMORAL NECROSIS FROM TWO MURINE BREAST ADENOCARCINOMAS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643206.

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Increased deposition and lysis of fibrin, associated with malignant tissue, has led to look for activators of both the coagulation and fibrinolytic systems produced by tumor cells. We report the evidences of a procoagblant activity (PA) in the extracts of intratumoral necrosis from two experimental breast adenocarcinomas in murine model (BALB/c). The tumors have different metastatic capacity (MC). M3 without MC and MM3 with high MC.The addition of the extracts to: 1- Normal Plasma, 2- Deficient substrates in coagulation factors, 3- Purified, fibrinogen (I), showed: 1- Shortening of the plasma recalcification time (PRT) and APTT, without ;modification on prothrombin time (PT), 2- Reduction of the PRT on deficient substrates in factors: VIII; VII; VII and X; V; V, VII and X; without modification on II deficient substrate, 3- No PA on I. Table:C: Control, s: seconds, m: minutes. The PA was not affected by heparin. The results suggest that the PA is independent of the presence of either factor VIII or factor VII (intrinsic or extrinsic pathway respectively), as well as presence of either factor V or factor X. Any effect was observed either on factor II deficient substrate or on I, so, there was no evidence of thrombin activity The PA could be act directly on factor II, suggesting that fibrin formation could be induced by a “non-classical” activation pathway. No significant differences (p&gt;0.5) in PA were observed between both tumoral necrosis extracts. The necrotic area in M3 (37%) is bigger than in MM3 (18%). So, much more PA could be present in MM3 and this could play a role in the MC of this tumor.
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Rivas, MA, M. Tkach, CJ Proietti, C. Rosemblit, W. Beguelin, V. Sundblad, MC Díaz Flaqué, EH Charreau, PV Elizalde, and R. Schillaci. "Tumor necrosis factor transactivates ErbB2 in breast cancer cells." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-4056.

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abla, hedia ben, Sonia Rekik, Soumaya Boussaid, Samia Jammali, Hela Sahli, Elhem Cheour, and Mohamed Elleuch. "AB0699 EFFECT OF SWITCHING BETWEEN TUMOR NECROSIS FACTOR INHIBITOR IN SPONDYLOARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3834.

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Pass, Harvey I., Steven Evans, Roger Perry, and Wilbert Matthews. "Kinetics of tumor necrosis factor production by photodynamic-therapy-activated macrophages." In OE/LASE '90, 14-19 Jan., Los Angeles, CA, edited by Thomas J. Dougherty. SPIE, 1990. http://dx.doi.org/10.1117/12.17660.

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Laabidi, S., S. Bizid, A. Ben Mahmoud, G. Mohamed, H. Ben Abdallah, MR Bouali, MN Abdelli, and E. Ghazouani. "Anti-Tumor Necrosis Factor Drug Response in Chronic Inflammatory Bowel Disease and Influencing Factors." In ESGE Days 2021. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1724752.

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Huang, Yun-Ju, Yao-Fan Fang, Shue-Fen Luo, Kuang-Hui Yu, Chang-Fu Kuo, Ping-Ha Tsai, and Yen-Fu Chen. "AB0383 LATENT TUBERCULOSIS INFECTION SHOULD BE MONITORED IN BOTH TUMOR NECROSIS FACTOR INHIBITORS AND NON-TUMOR NECROSIS FACTOR INHIBITORS IN BIOLOGICAL-NAïVE PATIENTS WITH RHEUMATOID ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3054.

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Rego, Stephen, Krista Ricci, Muthulekha Swamydas, and Didier Dreau. "Abstract 397: Soluble Tumor Necrosis Factor Receptor shed by breast tumor cells modulates macrophage migration." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-397.

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Iwona, Grądzka, Sikorska Katarzyna, and Brzóska Kamil. "Interference of Silver Nanoparticles with Tumor Necrosis Factor Action in Epithelial Cells." In The 2nd World Congress on Recent Advances in Nanotechnology. Avestia Publishing, 2017. http://dx.doi.org/10.11159/icnb17.116.

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Membriani, Evangelina, Erika Cuenca, Leticia Limongi, Ana Putruele, and Carlos Luna. "Latent tuberculosis screening and entering antibody therapy monoclonares against tumor necrosis factor." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2701.

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Reports on the topic "Tumor necrosis factor"

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Larrick, James W., Vera Morhenn, Yawen L. Chiang, and Tim Shi. Activated Langerhans Cells Release Tumor Necrosis Factor. Fort Belvoir, VA: Defense Technical Information Center, January 1988. http://dx.doi.org/10.21236/ada206646.

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Gao, Li-nan, Lian-gang Ge, Ming-zhe Zhu та Xin-xin Yao. Association between tumor necrosis factor α and uterine fibroids: a protocol of systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, липень 2020. http://dx.doi.org/10.37766/inplasy2020.7.0010.

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Li, Peng, and Junjun Liu. Effect of tumor necrosis factor inhibitors on the risk of adverse cardiovascular events in patients with psoriasis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0090.

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Review question / Objective: Previous studies have indicated a cardioprotective effect of tumor necrosis factor inhibitor (TNFi) therapy in adult patients with psoriasis (Pso). However, most were retrospective studies, and the association between cardiometabolic comorbidities and major adverse cardiovascular events (MACE) has not been validated in randomized controlled trials (RCTs). Condition being studied: Because the available evidence has recently increased, we performed the present updated meta-analysis and meta-regression of cohort studies and RCTs to evaluate whether TNFi therapy can decrease the risk of MACE among patients with Pso and to assess the associations between cardiometabolic comorbidities and MACE.
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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Factor-Related Apoptosis Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada532993.

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Borra, Himabindu, Daniel F. Battafarano, Ramon Arroyo, Michael J. Morris, Michelle Sit, and Gerald Merrill. Reliability of Tuberculosis Screening Test in Patients Receiving Tumor Necrosis Factor Antagonist Therapy in a United States Rheumatology Clinic. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada577631.

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Ni, Xiaofeng, and Lingli Zhang. Efficacy and Safety of Anti-Tumor Necrosis Factor Alpha in Very Early Onset Inflammatory Bowel Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2024. https://doi.org/10.37766/inplasy2024.12.0012.

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กาญจนทัต, อภิชาติ. ความเป็นพิษและการเหนี่ยวนำการตายแบบอะโพโทซิสต่อเซลล์มะเร็ง โดยเพปไทด์จากเกสรผึ้งพันธุ์ Apis mellifera. สถาบันวิจัยเทคโนโลยีชีวภาพและวิศวกรรมพันธุศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2018. https://doi.org/10.58837/chula.res.2018.100.

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งานวิจัยนี้เตรียมโปรตีนไฮโดรไลเสตจากเกสรผึ้งพันธุ์ ที่ได้จากปฏิกิริยาย่อยสลายด้วยเอนไซม์ 3 ชนิด ได้แก่ แอลคาเลส ฟลาโวไซม์ และนิวเทรส พบว่าเมื่อใช้นิวเทรสในอัตราส่วนของเอนไซม์ต่อสับสเตรต 1:1 (NH1) โดยปริมาตร จะให้แสดงค่าการยับยั้งการสร้างอนุมูลอิสระด้วยวิธีไนตริกออกไซต์ได้ดีที่สุด คัดแยกเพปไทด์ที่มีขนาดโมเลกุลต่ำกว่า 0.65 กิโลดาลตัน (MW1) มีฤทธิ์ในการขจัดอนุมูลอิสระไนตริกออกไซด์ได้ดีที่สุด จากนั่นได้ทำการตรวจสอบความเป็นพิษของ MW1 ด้วยวิธี MTT และตรวจสอบ ผลการยับยั้งการสร้างไนตริกออกไซด์ในเซลล์แมคโครฟาจ RAW 264.7 ที่ถูกกระตุ้นด้วยไลโปโพลิแซคคาไรด์ พบว่า MW1 ไม่มีความเป็นพิษต่อเซลล์ และมีฤทธิ์ในการยับยั้งการสร้างไนตริกออกไซด์ ผลการแสดงออกของยีนที่เกี่ยวของกับการอักเสบ พบว่า MW1 มีฤทธิ์ในการยับยั้งการแสดงออกของยีน inducible nitric oxide synthase (iNOS) Cyclooxygenase-2 (COX-2) Interleukin-6 (IL-6) และ Tumor necrosis factor alpha (TNF-α) จากนั้นนำ MW1 ไปทำบริสุทธิ์ด้วยเทคนิคโครมาโตกราฟีของเหลวสมรรถนะสูง สามารถแยกเพปไทด์ได้ทั้งหมด 6 พีค (H1-6) โดยที่ H2, H3 และ H4 แสดงค่าการยับยั้งการสร้างอนุมูลอิสระด้วยวิธีไนตริกออกไซด์ได้ดีที่สุด และนำเพปไทด์ที่ได้ไปพิสูจน์เอกลักษณ์ด้วยเทคนิคแมสสเปกโตรเมตรีพบเพปไทด์ทั้งหมด 7 สาย จากผลการศึกษาดังกล่าวแสดงให้เห็นว่าฤทธิ์ต้านการอักเสบของเพปไทด์จากเกสรผึ้งพันธุ์ สามารถนำไปประยุกต์ใช้ในอุสาหกรรมทางการแพทย์ เภสัชกรรมและผลิตภัณฑ์เครื่องสำอางต่อไป
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8

พงษ์เลาหพันธุ์, ศุภวิวัธน์, та ธีรพงศ์ ยะทา. การพัฒนาพาหะนำส่งยีนเหนี่ยวนำการตายของเซลล์แบบอะพอพโทซิสระดับนาโน เพื่อการคุมกำเนิดสัตว์เพศผู้แบบไม่ผ่าตัดทำหมัน : ต้นแบบเพื่อการคุมจำนวนประชากรสุนัขและแมวจรจัด. คณะสัตวแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2019. https://doi.org/10.58837/chula.res.2019.42.

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การศึกษาวิจัยนี้มีวัตถุประสงค์ เพื่อตรวจสอบการนำไปใช้ของอนุภาคไคโตซานระดับนาโนที่ถูกดัดแปลงให้มีคุณสมบัติเป็นตัวนำส่งยีนเหนี่ยวนำการตายแบบอะพอพโทซิสเข้าสู่เซลล์อัณฑะที่มีตัวรับฮอร์โมนโกนาโดโทรปินรีลิสซิ่ง โดยการออกแบบตัวนำส่งยีนนี้สามารถนำไปใช้ประโยชน์ในการทำหมันสัตว์เพศผู้แบบไม่ผ่าตัด การศึกษานี้ได้มีการรายงานผลของอนุภาคไคโตซานระดับนาโนเชื่อมติดกับฮอร์โมนโกนาโดโทรปินรีลิสซิ่ง (Gonadotropin Releasing Hormone-modified Chitosan; GnRH-CS) เพื่อนำส่งยีนอย่างมีเป้าหมาย และการใช้เปปไทด์โกนาโดโทรปินรีลิสซิ่งในการระบุเป้าหมายการนำส่งยีนไปสู่เซลล์ที่มีตัวรับฮอร์โมนโกนาโดโทรปินรีลิสซิ่ง (GnRH receptor; GnRHR) จากการศึกษาในห้องปฏิบัติการ (In vitro study) พบว่าอนุภาค GnRH-CS สามารถนำส่งยีนรายงานผล (Green Fluorescent Protein; GFP และ Luciferase; LUC) ไปสู่เซลล์เพาะเลี้ยงจากเซลล์ไตของตัวอ่อนมนุษย์ (Human Embryonic Kidney cell line) ที่มีการดัดแปลงให้มี GnRHR เพื่อใช้เป็นเซลล์จำลองที่มีการแสดง GnRHR และเซลล์สืบพันธุ์เพศผู้จากหนูเมาส์ (Spermatogonia cells; GC-1 cell) ได้อย่างจำเพาะ สำหรับการศึกษาภายในร่างกายสัตว์ (In vivo study) ได้มีการใช้ยีน Tumor Necrosis Factor alpha (TNF-alpha) เพื่อเหนี่ยวนำการตายในเซลล์อัณฑะของหนูแรท โดยการฉีดสารเข้าอัณฑะโดยตรง (Intra-testicular injection) ผลการศึกษาพบว่ามีการตายของเซลล์อัณฑะ (จากการตรวจทางจุลพยาธิวิทยา และการตรวจคลื่นเสียงความถี่สูงหรืออัลตราซาวน์) มีการลดลงอย่างมีนัยสำคัญทางสถิติของขนาดอัณฑะ (จากการตรวจทางกายภาพ การวัดด้วยคาลิปเปอร์แบบดิจิตอล และเครื่องชั่งน้ำหนักแบบดิจิตอล) ไม่พบผลข้างเคียงหลังการฉีด และพบว่ายังมีระดับฮอร์โมนเทสโทสเตอโรนในเลือดคงที่ (จากการตรวจด้วยหลักการ chemiluminescent microparticle immunoassay; CMIA) สรุปได้ว่างานวิจัยนี้สามารถนำไปประยุกต์ใช้ในการทำหมันสัตว์เพศผู้แบบไม่ผ่าตัด พบว่าวิธีนี้ช่วยลดการเกิดผลข้างเคียงจากการฉีดด้วยสารทำหมันอื่นที่มีรายงานก่อนหน้า
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9

Dotsenko, S. S., L. N. Shilova, A. S. Trofimenko, S. A. Bedina, E. A. Tikhomirova та M. A. Mamus. The role of cytokines in predicting the effectiveness of combined treatment with tumor necrosis factor α inhibitors in rheumatoid arthritis. ООО "ИМА-Пресс", 2018. http://dx.doi.org/10.18411/1995-4484-2018-56-33-17.

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10

Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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