Literatura académica sobre el tema "Tumor-inflammation"
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Artículos de revistas sobre el tema "Tumor-inflammation"
Dilmac, Sayra y Gamze Tanriover. "Tumor Biology and Inflammation." Journal of Pediatric Oncology 2, n.º 2 (20 de enero de 2015): 84–93. http://dx.doi.org/10.14205/2309-3021.2014.02.02.2.
Texto completoRay, L. B. "Inflammation and Tumor Progression". Science's STKE 2007, n.º 394 (3 de julio de 2007): tw246. http://dx.doi.org/10.1126/stke.3942007tw246.
Texto completoMaru, Yoshiro. "Inflammation in tumor progression". Folia Pharmacologica Japonica 138, n.º 4 (2011): 155–60. http://dx.doi.org/10.1254/fpj.138.155.
Texto completoLang, Florian y Christos Stournaras. "Serum and glucocorticoid inducible kinase, metabolic syndrome, inflammation, and tumor growth". HORMONES 12, n.º 2 (15 de abril de 2013): 160–71. http://dx.doi.org/10.14310/horm.2002.1401.
Texto completoLiu, Chunxiao, Jiayi Li, Wenjing Shi, Liujia Zhang, Shuang Liu, Yingcong Lian, Shujuan Liang y Hongyan Wang. "Progranulin Regulates Inflammation and Tumor". Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry 19, n.º 2 (8 de junio de 2020): 88–102. http://dx.doi.org/10.2174/1871523018666190724124214.
Texto completoLin, Qing, Shi Jin, Mei Han, Wenxin Zheng, Jiaming Liu y Xiaolong Wei. "Inflammation in the Tumor Microenvironment". Journal of Immunology Research 2018 (24 de junio de 2018): 1–2. http://dx.doi.org/10.1155/2018/1965847.
Texto completoSchmid, Michael C. y Judith A. Varner. "Myeloid cells in tumor inflammation". Vascular Cell 4, n.º 1 (2012): 14. http://dx.doi.org/10.1186/2045-824x-4-14.
Texto completoYang, L. y M. Karin. "Roles of tumor suppressors in regulating tumor-associated inflammation". Cell Death & Differentiation 21, n.º 11 (5 de septiembre de 2014): 1677–86. http://dx.doi.org/10.1038/cdd.2014.131.
Texto completoGarrity, James A. "Not a Tumor-Nonspecific Orbital Inflammation". Journal of Neurological Surgery Part B: Skull Base 82, n.º 01 (febrero de 2021): 096–99. http://dx.doi.org/10.1055/s-0040-1722636.
Texto completoLI, Ping y Jie-jun WANG. "Inflammation and tumor metastasis: recent progress". Academic Journal of Second Military Medical University 31, n.º 1 (25 de abril de 2011): 84–87. http://dx.doi.org/10.3724/sp.j.1008.2011.00084.
Texto completoTesis sobre el tema "Tumor-inflammation"
Huang, Hua. "Endothelial activation and inflammation in the tumor microenvironment". Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-247889.
Texto completoDe, Cock Jasmine M. (Jasmine Morgan). "Inflammation triggers Zeb1-dependent escape from tumor dormancy". Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104098.
Texto completoThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (pages 167-181).
Metastasis-related mortality for breast cancer patients often occurs many years after treatment of the primary tumor. Inflammation, through the orchestra of immune cells and released inflammatory cytokines, can predispose certain tissues to cancer development and can create a favorable environment for metastatic outgrowth. I evaluated whether lipopolysaccharide (LPS) could induce an inflammatory response, leading to the activation of the cell-biological epithelial-mesenchymal transition (EMT) program in dormant disseminated cancer cells in vivo, and subsequent metastatic outgrowth. To model metastatic cellular dormancy, I used a dormant subpopulation of cells (D2A1-d) that were enriched for in vivo from the highly metastatic carcinoma cell line D2A1, that was derived from spontaneous murine mammary tumor. The ability of the EMT program to awaken dormant disseminated D2A1-d cells was directly assessed in vivo, which resulted in the formation of macro-metastases following a transient induction of either the EMT-transcription factor Snail or Zeb1. Furthermore, the transient induction of Zeb1 led to the generation of CD29+ CD24- metastasis-initiating cells. In mice bearing dormant disseminated D2A1-d cells, my findings demonstrated that LPS-treatment resulted in the awakening of D2A1-d cells and metastatic outgrowth in the lungs and bone. The awakening of dormant disseminated D2A1-d cells was dependent, albeit through unknown mechanism, on the presence of neutrophils. The LPS-mediated awakening of dormant disseminated cancer cells was also dependent upon the activation of the EMT-inducing transcription factor Zeb1 in the D2A1-d cells. In conclusion, my thesis work demonstrated that inflammation can trigger the escape of metastatic dormancy in vivo.
by Jasmine M. De Cock.
Ph. D.
Nygren, Emma. "The role of Sema3A in inflammation mediated tumor progressions". Thesis, KTH, Skolan för bioteknologi (BIO), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-172790.
Texto completoMånga olika sorters celler är närvarande i tumörers mikromiljö och immunceller utgör en stor andel av dessa. Makrofager är centrala spelare o tumörimmunförsvaret och dessa kan indelas i olika aktiveringsgrader eller fenotyper, M1 eller M2 makrofager. M1 polariserade makrofager är tumörsuppressiva medan M2 makrofager bidrar till tumörtillväxt. De faktorer som reglerar skiftningen mellan M1 och M2 fenotyperna är under utredning. Vårt labb har identifierat att Immunsemaforinen 3A (Sema3A) spelar en roll i att reglera ackumuleringen av antitumorala M1 makrofager vilket leder till hämmad tumörtillväxt. Med denna information som bakgrund har detta examensarbete fokuserat på Sema3As roll i tumörmikromiljön. Med hjälp av lentivirusmedierad genterapi skapades en tumörcellinje som uttrycker shRNA mot Sema3AmRNA. Denna cellinjes visade 72% lägre Sema3A mRNA uttryck jämfört med kontorll och utvärderades sedan in vivo genom att följa tumörtillväxten i BALB/c mushonor. Immuncellsammansättningen i tumörerna analyserades sedan med hjälp av flödescytometri. Resultaten från in vivo experimentet visar att endogent Sema3A har en begränsad effekt på tumörutvecklingen. En något mer tumörgynnande immunprofil observerades i de tumörer där Sema3A uttryck var minskat. Utöver detta skapades också ett lentivirus för att transducera celler så att de överuttrycker Sema3A under en passande promotor för systemisk tillförsel.
Ng, Bernice Yu Jing. "Chronic Inflammation-Driven Tumor Promotion Asociated with CD8+ T Cells". Yale University, 2008. http://ymtdl.med.yale.edu/theses/available/etd-08232007-122524/.
Texto completoDieterich, Lothar. "Molecular Regulation of Inflammation and Angiogenesis in the Tumor Microenvironment". Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-152257.
Texto completoMa, Xiaojun. "Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth". Kyoto University, 2016. http://hdl.handle.net/2433/215461.
Texto completoKyoto University (京都大学)
0048
新制・課程博士
博士(医科学)
甲第19635号
医科博第73号
32671
京都大学大学院医学研究科医科学専攻
(主査)教授 妹尾 浩, 教授 渡邊 直樹, 教授 椛島 健治
学位規則第4条第1項該当
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.
Texto completoKumari, Vandana. "Mechanisms underlying the regulatory function of tumor necrosis factor-alpha in skin inflammation". Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17389.
Texto completoThe skin is the largest organ of an individuum and builds the barrier for a host against the environment. Skin barrier disruption by exogenous or endogenous stimuli can lead to skin inflammation. As a consequence, irritant or atopic eczema, frequent skin diseases, may evolve. Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine which plays a central role in inflammatory processes. The main aim of this thesis was to clarify whether and how endogenous TNF-α is contributing to skin inflammation driven by exogenous and endogenous triggers. The role of endogenous TNF-α was studied using TNF knockout (-/-) mice. In an irritation model, chemical and physical stimuli were applied on to mouse skin. Thymic stromal lymphopoietin (TSLP) was significantly induced by the used irritants. This TSLP induction was independent from endogenous TNF-α proven by using TNF-/- mice. Next the role of TNF-α in atopic dermatitis (AD) promoting an allergic skin inflammation was investigated. TNF-/- mice developed more severe AD compared to the wildtype mice and TSLP was significantly increased and correlated with the severity of the eczema. To prove the pathophysiological role of TSLP for AD progression, TNF-/- mice were pretreated with an TSLP antibody. Indeed, these mice developed less AD symptoms compared to the control mice. Mast cells (MCs) were also significantly increased in lesional skin in the AD model and moreover, correlated with AD severity, but also with TSLP expression.
CONSONNI, FRANCESCA MARIA. "Inflammation and cancer: relevance of myeloid cells recruitment and plasticity in tumor biology". Doctoral thesis, Università del Piemonte Orientale, 2017. http://hdl.handle.net/11579/86903.
Texto completoF, Consonni. "Inflammation and cancer: relevance of myeloid cells recruitment and plasticity in tumor biology". Doctoral thesis, Università del Piemonte Orientale, 2017. http://hdl.handle.net/11579/96173.
Texto completoLibros sobre el tema "Tumor-inflammation"
S, Grewal Iqbal, ed. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.
Buscar texto completoS, Grewal Iqbal, ed. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.
Buscar texto completoMarialuisa, Melli y Parente Luca, eds. Cytokines and lipocortins in inflammation and differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of IL-1, TNF, and Lipocortins in Inflammation and Differentiation, held in Siena, Italy, October 22-25, 1989. New York, NY: Wiley-Liss, 1990.
Buscar texto completoHarald, Tschesche, ed. Proteinases in inflammation and tumor invasion: Review articles including those from an international conference, Bielefeld, Federal Republic of Germany, March 14-16, 1985. Berlin: De Gruyter, 1986.
Buscar texto completoE, Sim, ed. Humoral factors. Oxford: IRL Press at Oxford University Press, 1993.
Buscar texto completoDougan, Michael Lawrence. Balancing oncogenic inflammation and anti-tumor immunity in the development of novel immune therapies for cancer. 2009.
Buscar texto completoGrewal, Iqbal S. Therapeutic Targets of the TNF Superfamily. Springer London, Limited, 2009.
Buscar texto completoGrewal, Iqbal S. Therapeutic Targets of the TNF Superfamily: Volume 647. Springer, 2010.
Buscar texto completoTschesche, Harald. Proteinases in Inflammation and Tumor Invasion: Review Articles Incl. Those from an Internat. Conference, Bielefeld, March 14 - 16 1985. De Gruyter, Inc., 1986.
Buscar texto completoTschesche, Harald. Proteinases in inflammation and tumor Invasion: Review articles incl. those from an internat. conference, Bielefeld, March 14 - 16 1985. De Gruyter, Inc., 2020.
Buscar texto completoCapítulos de libros sobre el tema "Tumor-inflammation"
Li, Yan, Xiao-yu R. Song y Marian T. Nakada. "Interplay between inflammation and tumor angiogenesis". En Cancer and Inflammation, 99–121. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7861-6_5.
Texto completoOstrand-Rosenberg, Suzanne y Pratima Sinha. "Inflammation, Tumor Progression, and Immune Suppression". En The Tumor Immunoenvironment, 177–96. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6217-6_7.
Texto completoOhsawa, Shizue y Tatsushi Igaki. "Non-autonomous Tumor Progression by Oncogenic Inflammation". En Chronic Inflammation, 211–22. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5_17.
Texto completoOkada, Futoshi. "Inflammation as a Niche for Tumor Progression". En Cancer and Inflammation Mechanisms, 149–64. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118826621.ch11.
Texto completoHan, Weiguo, Shereen A. Allam y Sherine F. Elsawa. "GLI2-Mediated Inflammation in the Tumor Microenvironment". En Advances in Experimental Medicine and Biology, 55–65. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44518-8_5.
Texto completoLin, E., S. E. Calvano y S. E. Lowry. "Tumor Necrosis Factor Receptors in Systemic Inflammation". En Immune Response in the Critically Ill, 365–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-57210-4_24.
Texto completoSica, Antonio y Chiara Porta. "Role of Tumor-Associated Macrophages (TAM) in Cancer Related Inflammation". En Tumor Microenvironment, 77–98. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470669891.ch5.
Texto completoOft, Martin. "IL-23 orchestrates the switch from tumor immune surveillance to tumor-promoting inflammation". En Th 17 Cells: Role in Inflammation and Autoimmune Disease, 161–72. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8681-8_14.
Texto completoReichle, Albrecht y Gerhard C. Hildebrandt. "The Comparative Uncovering of Tumor Systems Biology by Modularly Targeting Tumor-Associated Inflammation". En From Molecular to Modular Tumor Therapy, 287–303. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9531-2_13.
Texto completoRibatti, Domenico. "The Contribution of Immune Cells to Angiogenesis in Inflammation and Tumor Growth". En Inflammation and Angiogenesis, 27–84. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-68448-2_7.
Texto completoActas de conferencias sobre el tema "Tumor-inflammation"
Jungnickel, Christopher, Lina Bittigkoffer, Andreas Kamyschnikow, Christian Herr, Robert Bals y Christoph Beisswenger. "IL-17C promotes tumor-associated inflammation and lung tumor growth". En ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa1529.
Texto completoCampisi, Marco, Shriram K. Sundararaman, Shunsuke Kitajima, Valeria Chiono, Roger D. Kamm y David A. Barbie. "Abstract 958: Tumor-vascular interactions promote STING-driven inflammation in the tumor microenvironment". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-958.
Texto completoCampisi, Marco, Shriram K. Sundararaman, Shunsuke Kitajima, Valeria Chiono, Roger D. Kamm y David A. Barbie. "Abstract 958: Tumor-vascular interactions promote STING-driven inflammation in the tumor microenvironment". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-958.
Texto completoKarin, Michael. "Abstract SY19-01: Tumor-elicited inflammation in colorectal cancer". En 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-sy19-01.
Texto completoLevi, Oshrat. "HSF1 promotes inflammation induced tumor development through ECM remodeling". En European Light Microscopy Initiative 2021. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.elmi2021.68.
Texto completoFrancescone, Ralph, Debora Vendramini-Costa, Oxana Dmitrieva, Vivi Hou, David Posocco y Sergei Grivennikov. "Abstract 3183: Role of danger signals in tumor elicited inflammation". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3183.
Texto completoSmith, Courtney, Mee-Young Chang, Hollie Flick, James DuHadaway, Laura Mandik-Nayak, Lisa Laury-Kleintop, Katherine Parker et al. "Abstract 295: IDO drives tumor-promoting, pathogenic inflammation in lung". En 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.am2012-295.
Texto completoSchmid, Tobias, Daniela Rübsamen, Johanna S. Blees, Magdalena M. Bajer, Larissa Milke, Kathrin Schulz, Curtis J. Henrich, James B. McMahon, Nancy H. Colburn y Bernhard Brüne. "Abstract A15: Inflammation-dependent deregulation of the tumor suppressor Pdcd4". En Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a15.
Texto completoKato, Takuma, Nishikawa Hiroyoshi, Wang Linan, Mitusi Jun, Maeda Yuka, Shiku Hiorshi y Shiku Hiorshi. "Abstract 5323: Distinct roles of IL-17A in inflammation-induced tumor development and tumor immunosurveillance". En 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.am10-5323.
Texto completoCarlson, Lena-Maria, Agnes Rasmuson, Lova Segerstrom, Baldur Sveinbjornsson y Per Kogner. "Abstract LB-496: Low-dose aspirin targets tumor-associated inflammation and delays neuroblastoma tumor growthin vivo". En 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-lb-496.
Texto completoInformes sobre el tema "Tumor-inflammation"
Diaz-Meco, Maria T. Inflammation in Prostate Carcinogenesis: Role of the Tumor Suppressor Par-4. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2012. http://dx.doi.org/10.21236/ada576664.
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