Relevant bibliographies by topics / Tumor-inflammation

Contents

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

Academic literature on the topic 'Tumor-inflammation'

Author: Grafiati
Published: 1 April 2023

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Journal articles on the topic "Tumor-inflammation"

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Dilmac, Sayra, and Gamze Tanriover. "Tumor Biology and Inflammation." Journal of Pediatric Oncology 2, no. 2 (January 20, 2015): 84–93. http://dx.doi.org/10.14205/2309-3021.2014.02.02.2.

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Ray, L. B. "Inflammation and Tumor Progression." Science's STKE 2007, no. 394 (July 3, 2007): tw246. http://dx.doi.org/10.1126/stke.3942007tw246.

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Maru, Yoshiro. "Inflammation in tumor progression." Folia Pharmacologica Japonica 138, no. 4 (2011): 155–60. http://dx.doi.org/10.1254/fpj.138.155.

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Lang, Florian, and Christos Stournaras. "Serum and glucocorticoid inducible kinase, metabolic syndrome, inflammation, and tumor growth." HORMONES 12, no. 2 (April 15, 2013): 160–71. http://dx.doi.org/10.14310/horm.2002.1401.

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Liu, Chunxiao, Jiayi Li, Wenjing Shi, Liujia Zhang, Shuang Liu, Yingcong Lian, Shujuan Liang, and Hongyan Wang. "Progranulin Regulates Inflammation and Tumor." Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry 19, no. 2 (June 8, 2020): 88–102. http://dx.doi.org/10.2174/1871523018666190724124214.

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Progranulin (PGRN) mediates cell cycle progression and cell motility as a pleiotropic growth factor and acts as a universal regulator of cell growth, migration and transformation, cell cycle, wound healing, tumorigenesis, and cytotoxic drug resistance as a secreted glycoprotein. PGRN overexpression can induce the secretion of many inflammatory cytokines, such as IL-8, -6,-10, TNF-α. At the same time, this protein can promote tumor proliferation and the occurrence and development of many related diseases such as gastric cancer, breast cancer, cervical cancer, colorectal cancer, renal injury, neurodegeneration, neuroinflammatory, human atherosclerotic plaque, hepatocarcinoma, acute kidney injury, amyotrophic lateral sclerosis, Alzheimer’s disease and Parkinson’s disease. In short, PGRN plays a very critical role in injury repair and tumorigenesis, it provides a new direction for succeeding research and serves as a target for clinical diagnosis and treatment, thus warranting further investigation. Here, we discuss the potential therapeutic utility and the effect of PGRN on the relationship between inflammation and cancer.
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Lin, Qing, Shi Jin, Mei Han, Wenxin Zheng, Jiaming Liu, and Xiaolong Wei. "Inflammation in the Tumor Microenvironment." Journal of Immunology Research 2018 (June 24, 2018): 1–2. http://dx.doi.org/10.1155/2018/1965847.

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Schmid, Michael C., and Judith A. Varner. "Myeloid cells in tumor inflammation." Vascular Cell 4, no. 1 (2012): 14. http://dx.doi.org/10.1186/2045-824x-4-14.

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Yang, L., and M. Karin. "Roles of tumor suppressors in regulating tumor-associated inflammation." Cell Death & Differentiation 21, no. 11 (September 5, 2014): 1677–86. http://dx.doi.org/10.1038/cdd.2014.131.

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Garrity, James A. "Not a Tumor-Nonspecific Orbital Inflammation." Journal of Neurological Surgery Part B: Skull Base 82, no. 01 (February 2021): 096–99. http://dx.doi.org/10.1055/s-0040-1722636.

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Abstract Objective This study was aimed to illustrate the features and complexities of nonspecific orbital inflammation via discussion of two representative cases. Design Present study is a retrospective case review. Setting The study was conducted at a tertiary care medical center. Participants Two patients with nonspecific orbital inflammation were participants of this retrospective study. Main Outcome Measures Outcome of the study was disease-free patients and off all medications. Results At follow-up, both patients are disease free and off all medications. Conclusion Surgery plays a diagnostic and therapeutic role. While the clinical subtype is important for differential diagnosis and symptomatic treatment, the histologic subtype is similarly important. For inflammatory dacryoadenitis, surgery can be therapeutic. For extensive granulomatosis with polyangiitis, debulking surgery may allow better penetration of medications, especially rituximab.
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LI, Ping, and Jie-jun WANG. "Inflammation and tumor metastasis: recent progress." Academic Journal of Second Military Medical University 31, no. 1 (April 25, 2011): 84–87. http://dx.doi.org/10.3724/sp.j.1008.2011.00084.

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Dissertations / Theses on the topic "Tumor-inflammation"

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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.

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Tumors are composed not only of malignant cells, but also of various types of normal cells, including vascular cells and infiltrating immune cells, which drive tumor development and progression. The tumor vasculature is abnormal and dysfunctional due to sustained tumor angiogenesis driven by high levels of pro-angiogenic factors. Proteins differentially expressed in tumor vessels affect vascular function and the tumor microenvironment and may serve as targets for therapy. The tumor is also a site of sustained chronic inflammation. The recruitment and activation of inflammatory cells significantly influence tumor progression and regression. Targeting molecules regulating tumor angiogenesis and inflammation in the tumor microenvironment is therefore a promising strategy for the treatment of cancer. This thesis is aiming to understand and investigate the molecular regulation of these two processes in tumors. αB-crystallin is a heat shock protein previously proposed as a target for cancer therapy due to its role in increasing survival of tumor cells and enhancing tumor angiogenesis. In this thesis, we demonstrate a novel role of αB-crystallin in limiting expansion of CD11b+Gr1+ immature myeloid cells in pathological conditions, including tumor development. In addition, we show that αB-crystallin regulates leukocyte recruitment by promoting expression of adhesion molecules ICAM-1, VCAM-1 and E-selectin during TNF-α-induced endothelial activation. Therefore, targeting of αB-crystallin may influence tumor inflammation by regulating immature myeloid cell expansion and leukocyte recruitment. Abnormal, dysfunctional vessels are characteristic of glioblastomas, which are aggressive malignant brain tumors. We have identified the orphan G-protein coupled receptor ELTD1 as highly expressed in glioblastoma vessel and investigated its role in tumor angiogenesis. Interestingly, deficiency of ELTD1 was associated with increased growth of orthotopic GL261 glioma and T241 fibrosarcoma, but did not affect vessel density in any model. Further investigation is warranted to evaluate whether ELTD1 serves a suitable vascular target for glioblastoma treatment. Anti-angiogenic drugs targeting VEGF signaling is widely used in the clinic for various types of cancer. However, the influences of anti-angiogenic treatment on tumor inflammation have not been thoroughly investigated. We demonstrate that VEGF inhibits TNF-α-induced endothelial activation by repressing NF-κB activation and expression of chemokines involved in T-cell recruitment. Sunitinib, a small molecule kinase inhibitor targeting VEGF/VEGFR2 signaling increased expression of chemokines CXCL10, CXCL11, and enhanced T-lymphocyte infiltration into tumors. Our study suggests that anti-angiogenic therapy may improve immunotherapy by enhancing endothelial activation and facilitating immune cell infiltration into tumors.
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De, 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.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.
This 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.
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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.

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In the tumor microenvironment there are many different cell types present and among these, immune cells display a large proportion. Central players in the tumor immunity are macrophages that come in two different phenotypes, the M1 and M2 macrophages. M1 polarized macrophages are tumor suppressive while M2 polarized macrophages support tumor growth. The factors that contribute to the skewing of macrophages from one phenotype to another are under investigation. Interestingly, our lab has identified Immune Semaphorin 3A (Sema3A) as a participating plaer in regulating the accumulation of anti-tumoral M1 macrophages leading to a suppression of tumor growth.   In light of these data this thesis has focused on the role of endogenous Sema3A in the tumor microenvironment. A tumor cell line expressing shRNA against Sema3A mRNA was generated using lentiviral mediated gene therapy. This knockdoen cell line showed 72% lower mRNA expression compared to control and was evaluated in vivo by monitoring tumor progression in female BALB/c mice. The immune cell composition of the tumors was analysed using flow cytometry. The results from the in vivo experiment show that endogenous Sema3A has a limited effect on tumor progression. A slight shift to a more tumor supportive immune profile was observed in the knockdown tumors. Moreover, a virus for transducing cells to overecpress Sema3A under asuitable promoter for systemic delivery was generated.
Många 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.
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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/.

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Chronic inflammation is associated with carcinoma development in several clinical settings, and we sought to investigate the role of T cells in this phenomenon using the DMBA/TPA two-stage chemical carcinogenesis protocol. We demonstrate that, paradoxical to models of immunosurveillance, wild-type (WT) mice have a markedly higher rate of tumor formation relative to strains lacking CD8+ T cells. Adoptive transfers of antibody-coated magnetic bead-enriched peripheral CD8+ T cells into TCRáâ-/- mice confirmed that the increased mean tumor area and progression to carcinoma was attributable to the presence of CD8+ T cells. All analyzed strains of mice in which the CD8 compartment was intact (WT, CD4-/-) showed significant increases in tumor susceptibility. Putative tumor-promoting (T-pro) cells (TCRáâ+CD8+CD44+CD62L- tumor infiltrating lymphocytes, TILs) were directly compared to their phenotypic equivalents in peripheral blood lymphocytes (PBLs). In WT and CD4-deficient mice, CD8+ TILs consistently revealed a markedly higher relative expression, by RT-PCR, of IFNã, TNFá and COX-2, and a striking decrease in expression of perforin. Cytokine-bead analysis (CBA) comparison of CD8+ and CD4+ TIL in tumors from WT mice confirmed the increased expression by the CD8+ TIL of IFNã and TNFá. To our knowledge, this is the first demonstration of increased carcinogenesis attributable to CD8+ TILs, characterized by their high IFNã, TNFá, and COX-2 production and defective perforin production relative to phenotypically equivalent PBLs. These studies may have mechanistic implications for the role of T cells in inflammation-associated carcinogenesis.
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Dieterich, 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.

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Tumor growth and progression not only depend on properties of the malignant cells but are strongly influenced by the tumor microenvironment. The tumor stroma consists of various cell types such as inflammatory cells, endothelial cells and fibroblasts, which can either inhibit or promote tumor growth. Consequently, therapeutic targeting of the tumor stroma is increasingly recognized as an important tool to fight cancer. Two particularly important processes that contribute to the pathology of most types of tumors are angiogenesis and inflammation. In order to target these processes specifically and efficiently, it is fundamental to identify and understand the factors and signaling pathways involved. This thesis initially describes the multiple functions of the small heat shock protein αB-crystallin in the tumor microenvironment. αB-crystallin was first identified in a screen of proteins specifically up-regulated in endothelial cells forming vessel-like structures. We found that αB-crystallin is expressed in a subset of tumor vessels and promotes angiogenesis by inhibiting endothelial apoptosis, suggesting that targeting of αB-crystallin might inhibit angiogenesis and thereby decrease tumor growth. However, we also discovered an important role of αB-crystallin in regulation of inflammatory processes. We show that αB-crystallin increases the surface levels of E-selectin, an important leukocyte-endothelial adhesion molecule. Thereby, αB-crystallin may alter leukocyte recruitment to inflamed tissues such as the tumor stroma. In addition, we found that αB-crystallin is expressed in immature myeloid cells that accumulate in the periphery and at the tumor site during tumor development. Importantly, lack of αB-crystallin resulted in increased accumulation of immature myeloid cells, which might increase tumor associated inflammation. Finally, through combining laser microdissection of vessels from human tissue and microarray analysis, we identified a gene expression signature specifically associated with vessels in high grade glioma. Blood vessels in malignant glioma are highly abnormal and contribute to the pathology of the disease. Thus, knowledge about the molecular set-up of these vessels might contribute to the development of future vascular normalizing treatments.
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Ma, 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.

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Final publication is available at http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=26018088
Kyoto 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
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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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Kumari, 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.

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Die Haut ist das größte Organ des Menschen und bildet die Barriere gegenüber Einwirkungen aus der Umwelt. Die Störung der Hautbarriere durch exogene und endogene Reize führt zu einer Entzündungsreaktion in der Haut. In der Folge können Hauterkrankungen wie die irritative oder Atopische Dermatitis entstehen. Der Tumor Nekrose Faktor-α (TNF-α) ist ein pleiotrop wirksames Zytokin, das eine zentrale Rolle bei entzündlichen Prozessen spielt. Ziel der vorgelegten Promotionsarbeit war zu untersuchen, ob und wie TNF-α zu Entzündungsgeschehen, ausgelöst durch exogene und endogene Faktoren, beiträgt. Die Bedeutung von TNF-α wurde in TNF-ko Mäusen in verschiedenen Hautmodellen untersucht. Für das Irritationsmodell wurden chemische und physikalische Reize verwendet. TSLP (Thymic stromal lymphopoietin) wurde durch die verschiedenen Stimuli signifikant induziert. Diese Induktion war unabhängig von der endogenen TNF-α Produktion, gezeigt durch den Einsatz von TNF- ko Mäusen . Da endogenes TNF-α für die Hautirritation keine notwendige Bedingung darstellte, wurde die Bedeutung von TNF-α bei der atopischen Dermatitis (AD) untersucht. TNF-α defiziente Mäuse zeigen verstärkt Ekzeme im Vergleich zu Wildtyp Mäusen. Die Behandlung von TNF-ko Mäusen mit einem TSLP Antikörper führte zu einer Verminderung des Ekzems. Mastzellen wurden vermehrt in läsionaler Haut gefunden und korrelierten mit dem Schweregrad des atopischen Ekzems sowie der TSLP-Expression.
The 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.
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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.

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F, 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.

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Books on the topic "Tumor-inflammation"

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S, Grewal Iqbal, ed. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.

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S, Grewal Iqbal, ed. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.

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Marialuisa, Melli, and 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.

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Harald, 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.

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E, Sim, ed. Humoral factors. Oxford: IRL Press at Oxford University Press, 1993.

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Dougan, Michael Lawrence. Balancing oncogenic inflammation and anti-tumor immunity in the development of novel immune therapies for cancer. 2009.

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Grewal, Iqbal S. Therapeutic Targets of the TNF Superfamily. Springer London, Limited, 2009.

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Grewal, Iqbal S. Therapeutic Targets of the TNF Superfamily: Volume 647. Springer, 2010.

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Tschesche, Harald. Proteinases in Inflammation and Tumor Invasion: Review Articles Incl. Those from an Internat. Conference, Bielefeld, March 14 - 16 1985. De Gruyter, Inc., 1986.

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Tschesche, Harald. Proteinases in inflammation and tumor Invasion: Review articles incl. those from an internat. conference, Bielefeld, March 14 - 16 1985. De Gruyter, Inc., 2020.

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Book chapters on the topic "Tumor-inflammation"

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Li, Yan, Xiao-yu R. Song, and Marian T. Nakada. "Interplay between inflammation and tumor angiogenesis." In Cancer and Inflammation, 99–121. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7861-6_5.

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Ostrand-Rosenberg, Suzanne, and Pratima Sinha. "Inflammation, Tumor Progression, and Immune Suppression." In The Tumor Immunoenvironment, 177–96. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6217-6_7.

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Ohsawa, Shizue, and Tatsushi Igaki. "Non-autonomous Tumor Progression by Oncogenic Inflammation." In Chronic Inflammation, 211–22. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5_17.

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Okada, Futoshi. "Inflammation as a Niche for Tumor Progression." In Cancer and Inflammation Mechanisms, 149–64. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118826621.ch11.

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Han, Weiguo, Shereen A. Allam, and Sherine F. Elsawa. "GLI2-Mediated Inflammation in the Tumor Microenvironment." In 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.

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Lin, E., S. E. Calvano, and S. E. Lowry. "Tumor Necrosis Factor Receptors in Systemic Inflammation." In 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.

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Sica, Antonio, and Chiara Porta. "Role of Tumor-Associated Macrophages (TAM) in Cancer Related Inflammation." In Tumor Microenvironment, 77–98. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470669891.ch5.

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Oft, Martin. "IL-23 orchestrates the switch from tumor immune surveillance to tumor-promoting inflammation." In 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.

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Reichle, Albrecht, and Gerhard C. Hildebrandt. "The Comparative Uncovering of Tumor Systems Biology by Modularly Targeting Tumor-Associated Inflammation." In From Molecular to Modular Tumor Therapy, 287–303. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9531-2_13.

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Ribatti, Domenico. "The Contribution of Immune Cells to Angiogenesis in Inflammation and Tumor Growth." In Inflammation and Angiogenesis, 27–84. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-68448-2_7.

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Conference papers on the topic "Tumor-inflammation"

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Jungnickel, Christopher, Lina Bittigkoffer, Andreas Kamyschnikow, Christian Herr, Robert Bals, and Christoph Beisswenger. "IL-17C promotes tumor-associated inflammation and lung tumor growth." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa1529.

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Campisi, Marco, Shriram K. Sundararaman, Shunsuke Kitajima, Valeria Chiono, Roger D. Kamm, and David A. Barbie. "Abstract 958: Tumor-vascular interactions promote STING-driven inflammation in the tumor microenvironment." In 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.

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Campisi, Marco, Shriram K. Sundararaman, Shunsuke Kitajima, Valeria Chiono, Roger D. Kamm, and David A. Barbie. "Abstract 958: Tumor-vascular interactions promote STING-driven inflammation in the tumor microenvironment." In 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.

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Karin, Michael. "Abstract SY19-01: Tumor-elicited inflammation in colorectal cancer." 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-sy19-01.

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Levi, Oshrat. "HSF1 promotes inflammation induced tumor development through ECM remodeling." In European Light Microscopy Initiative 2021. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.elmi2021.68.

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Francescone, Ralph, Debora Vendramini-Costa, Oxana Dmitrieva, Vivi Hou, David Posocco, and Sergei Grivennikov. "Abstract 3183: Role of danger signals in tumor elicited inflammation." In 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.

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Smith, 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." 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.am2012-295.

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Schmid, Tobias, Daniela Rübsamen, Johanna S. Blees, Magdalena M. Bajer, Larissa Milke, Kathrin Schulz, Curtis J. Henrich, James B. McMahon, Nancy H. Colburn, and Bernhard Brüne. "Abstract A15: Inflammation-dependent deregulation of the tumor suppressor Pdcd4." In 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.

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Kato, Takuma, Nishikawa Hiroyoshi, Wang Linan, Mitusi Jun, Maeda Yuka, Shiku Hiorshi, and Shiku Hiorshi. "Abstract 5323: Distinct roles of IL-17A in inflammation-induced tumor development and tumor immunosurveillance." 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.am10-5323.

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Carlson, Lena-Maria, Agnes Rasmuson, Lova Segerstrom, Baldur Sveinbjornsson, and Per Kogner. "Abstract LB-496: Low-dose aspirin targets tumor-associated inflammation and delays neuroblastoma tumor growthin vivo." 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-lb-496.

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Reports on the topic "Tumor-inflammation"

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Diaz-Meco, Maria T. Inflammation in Prostate Carcinogenesis: Role of the Tumor Suppressor Par-4. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada576664.

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