Journal articles: 'Tumor-inflammation'

1

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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Liu, Jingyi, Pengnian Lin, and Binhua Zhou. "Inflammation Fuels Tumor Progress and Metastasis." Current Pharmaceutical Design 21, no. 21 (June 9, 2015): 3032–40. http://dx.doi.org/10.2174/1381612821666150514105741.

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Bondar, Tanya, and Ruslan Medzhitov. "The Origins of Tumor-Promoting Inflammation." Cancer Cell 24, no. 2 (August 2013): 143–44. http://dx.doi.org/10.1016/j.ccr.2013.07.016.

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Mburu, Yvonne K., Jun Wang, Michelle A. Wood, William H. Walker, and Robert L. Ferris. "CCR7 Mediates Inflammation-Associated Tumor Progression." Immunologic Research 36, no. 1-3 (2006): 61–72. http://dx.doi.org/10.1385/ir:36:1:61.

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Pufnock, Jeff S., and Jay L. Rothstein. "Oncoprotein Signaling Mediates Tumor-Specific Inflammation and Enhances Tumor Progression." Journal of Immunology 182, no. 9 (April 20, 2009): 5498–506. http://dx.doi.org/10.4049/jimmunol.0801284.

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15

Jungnickel, C., L. Bittigkoffer, A. Kamyschnikow, C. Herr, R. Bals, and C. Beisswenger. "IL-17C promotes tumor-associated inflammation and lung tumor growth." European Journal of Cancer 61 (July 2016): S209. http://dx.doi.org/10.1016/s0959-8049(16)61738-0.

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Lu, Chih-hao, Da-Wei Yeh, Chao-Yang Lai, Yi-Ling Liu, and Tsung-Hsien Chuang. "DUB-3 regulation of tumor associated inflammation and tumor growth." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 73.16. http://dx.doi.org/10.4049/jimmunol.196.supp.73.16.

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Abstract The tumor microenvironment includes blood vessels, immune cells, fibroblasts, and tumor cells. Inflammation in tumor microenvironment leads to the initiation, promotion, invasion, and metastasis of cancer. Inflammation stimuli such as TNF-α, IL-1β and TLR ligands are capable of activating the NF-κB controlled inflammatory signaling in cancer cells. The activations by these stimuli are modulated by various signaling molecules including those control ubiquitination and deubiquitination in the NF-κB signaling pathway. The DUB-3, has been identified as a deubiquitinating enzyme that belongs to cytokine inducible DUBs. In this study, we investigated the function of DUB-3 in control of inflammatory responses in different cancer cells. Expression of DUB-3 in these cancer cells regulated IL-1β, LPS, and Pam3Cys induced cytokine and chemokine productions and generated favorable conditions for tumor growth. DUB-3 promoted in vivo tumorigenesis and tumor growth. H&E staining of tumor sections revealed higher leukocyte infiltration in the tumors. The expression of genes associated with inflammation were investigated, and higher expression of inflammatory cytokines and chemokines were observed in tumors. Taken together, these observations suggest that DUB-3 regulates tumor growth by modulating inflammatory associated function.

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Njunge, Lucy Wanjiru, Andreanne Poppy Estania, Yao Guo, Wanqian Liu, and Li Yang. "Tumor progression locus 2 (TPL2) in tumor-promoting Inflammation, Tumorigenesis and Tumor Immunity." Theranostics 10, no. 18 (2020): 8343–64. http://dx.doi.org/10.7150/thno.45848.

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Schmid, Michael C., and Judith A. Varner. "Myeloid Cells in the Tumor Microenvironment: Modulation of Tumor Angiogenesis and Tumor Inflammation." Journal of Oncology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/201026.

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Myeloid cells are a heterogeneous population of bone marrow-derived cells that play a critical role during growth and metastasis of malignant tumors. Tumors exhibit significant myeloid cell infiltrates, which are actively recruited to the tumor microenvironment. Myeloid cells promote tumor growth by stimulating tumor angiogenesis, suppressing tumor immunity, and promoting metastasis to distinct sites. In this review, we discuss the role of myeloid cells in promoting tumor angiogenesis. Furthermore, we describe a subset of myeloid cells with immunosuppressive activity (known as myeloid-derived suppressor cells). Finally, we will comment on the mechanisms regulating myeloid cell recruitment to the tumor microenvironment and on the potential of myeloid cells as new targets for cancer therapy.

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Varney, Michelle L., and Rakesh K. Singh. "The Role of Inflammation in Tumor Progression: Targeting Tumor-Associated Macrophages." Clinical Research and Regulatory Affairs 25, no. 3 (January 2008): 139–55. http://dx.doi.org/10.1080/10601330802208291.

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Gonda, Tamas A., Shuiping Tu, and Timothy C. Wang. "Chronic inflammation, the tumor microenvironment and carcinogenesis." Cell Cycle 8, no. 13 (July 2009): 2005–13. http://dx.doi.org/10.4161/cc.8.13.8985.

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Mantovani, Alberto. "Tumor-associated macrophages in cancer-related inflammation." Immunotherapy 3, no. 4s (April 2011): 21–22. http://dx.doi.org/10.2217/imt.11.32.

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Thakar, Sumit, SunilV Furtado, Nandita Ghosal, and AlangarS Hegde. "Intracranial germ cell tumor mimicking granulomatous inflammation." Neurology India 61, no. 4 (2013): 433. http://dx.doi.org/10.4103/0028-3886.117597.

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23

Warren, Jeffrey S. "Interleukins and Tumor Necrosis Factor in Inflammation." Critical Reviews in Clinical Laboratory Sciences 28, no. 1 (January 1990): 37–59. http://dx.doi.org/10.3109/10408369009105897.

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Luster, Michael I. "Editorial: Inflammation, Tumor Necrosis Factor, and Toxicology." Environmental Health Perspectives 106, no. 9 (September 1998): A418. http://dx.doi.org/10.2307/3434211.

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25

Dougan, Michael, and Glenn Dranoff. "Inciting inflammation: the RAGE about tumor promotion." Journal of Experimental Medicine 205, no. 2 (February 11, 2008): 267–70. http://dx.doi.org/10.1084/jem.20080136.

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Mechanisms of innate and adaptive immunity play a pivotal role in the development of cancer. Chronic inflammation can drive tumor development, but antitumor immunity can also restrict or even prevent tumor growth. New data show that feed-forward signals downstream of the receptor for advanced glycation end-products (RAGE) can fuel chronic inflammation, creating a microenvironment that is ideal for tumor formation.

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Maletzki, C., and J. Emmrich. "Inflammation and Immunity in the Tumor Environment." Digestive Diseases 28, no. 4-5 (2010): 574–78. http://dx.doi.org/10.1159/000321062.

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Michiels, C., C. Tellier, C. Graux, L. Finet, M. Raes, and O. Feron. "171: Cycling hypoxia amplifies tumor microenvironment inflammation." European Journal of Cancer 50 (July 2014): S38. http://dx.doi.org/10.1016/s0959-8049(14)50144-x.

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Gkretsi, Vasiliki, Lefteris C. Zacharia, and Triantafyllos Stylianopoulos. "Targeting Inflammation to Improve Tumor Drug Delivery." Trends in Cancer 3, no. 9 (September 2017): 621–30. http://dx.doi.org/10.1016/j.trecan.2017.07.006.

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Grossberg, A., E. G. Vichaya, D. L. Christian, J. M. Molkentine, D. Vermeer, P. Vermeer, J. H. Lee, C. J. Heijnen, A. Kavelaars, and R. Dantzer. "Tumor-associated fatigue develops independently of inflammation." Brain, Behavior, and Immunity 66 (November 2017): e6. http://dx.doi.org/10.1016/j.bbi.2017.07.035.

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30

Greten, Florian R. "The Iron y of Tumor-Induced Inflammation." Cell Metabolism 24, no. 3 (September 2016): 368–69. http://dx.doi.org/10.1016/j.cmet.2016.08.025.

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Nelson, Delia, and Ruth Ganss. "Tumor growth or regression: powered by inflammation." Journal of Leukocyte Biology 80, no. 4 (July 24, 2006): 685–90. http://dx.doi.org/10.1189/jlb.1105646.

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Shiralkar, Malan, Patrick McKenzie, Keisa Lynch, Ryan O'Hara, Ziga Cizman, and Michael Sossenheimer. "1368 Hilar Inflammation Mimicking a Klatskin Tumor." American Journal of Gastroenterology 114, no. 1 (October 2019): S756—S757. http://dx.doi.org/10.14309/01.ajg.0000595000.33414.4b.

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Arias, Jose-Ignacio, María-Angeles Aller, and Jaime Arias. "The use of inflammation by tumor cells." Cancer 104, no. 2 (2005): 223–28. http://dx.doi.org/10.1002/cncr.21165.

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Bitoux, Marie-Aude, and Ivan Stamenkovic. "Tumor-host interactions: the role of inflammation." Histochemistry and Cell Biology 130, no. 6 (October 25, 2008): 1079–90. http://dx.doi.org/10.1007/s00418-008-0527-3.

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Manshian, Bella B., Jennifer Poelmans, Shweta Saini, Suman Pokhrel, Julio Jiménez Grez, Uwe Himmelreich, Lutz Mädler, and Stefaan J. Soenen. "Nanoparticle-induced inflammation can increase tumor malignancy." Acta Biomaterialia 68 (March 2018): 99–112. http://dx.doi.org/10.1016/j.actbio.2017.12.020.

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Libreros, Stephania, Ramon Garcia-Areas, and Vijaya Iragavarapu. "Chitinase-3 like-protein-1 (CHI3L1) expression associated with pulmonary inflammation accelerates breast cancer metastasis (TUM7P.960)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 203.42. http://dx.doi.org/10.4049/jimmunol.192.supp.203.42.

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Abstract Disseminated metastasis accounts for a majority of breast cancer deaths. Recently, elevated serum levels of a glycoprotein known as chitinase-3 like-protein-1 (CHI3L1) has been correlated with poor prognosis in both breast cancer and asthmatic patients. We have combined mouse models of breast cancer and pulmonary inflammation to determine if CHI3L1 associated pulmonary inflammation accelerates metastasis. We found that allergic pulmonary inflammation significantly enhances primary tumor growth in 4T1, 4T07 and 67NR mammary tumors by 10-fold, while decreasing survival. 4T1 tumor bearers with allergic pulmonary inflammation showed a 100-fold increase in metastatic tumor formation. We also assessed CHI3L1 levels and myeloid cells in the lungs of wild type and CHI3L1 knockout mice with allergic pulmonary inflammation and 4T1 mammary tumors. CHI3L1 levels were higher in the lungs of mammary tumor bearers with allergic pulmonary inflammation and correlated with increased metastasis. Wild type mammary tumor bearers with allergic inflammation had higher numbers of myeloid cells in the lungs in comparison to CHI3L1 knockout tumor bearers with allergic pulmonary inflammation. CHI3L1 knockout mice tumor bearers had significantly fewer myeloid cells in the lungs, decreased tumor growth and metastasis, along with increased survival. We propose that increased CHI3L1 in the lungs attracts myeloid cells that promote tumor growth and breast cancer metastasis.

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Szabo, Peter M., Zhenhao Qi, Kim Zerba, Scott Ely, Robin Edwards, James Lu, James Cooley, Marian Navratil, Gillian L. Dalgliesh, and Neeraj Adya. "Association of an inflammatory gene signature with CD8 expression by immunohistochemistry (IHC) in multiple tumor types." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 2593. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.2593.

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2593 Background: A multiparameter tumor inflammation assay based on gene expression profiling (TIA-GEP) can extend the utility of IHC to interrogate the tumor microenvironment (TME). Using CD8 expression assessed by IHC (CD8-IHC) as a surrogate for inflammation, statistical modelling was used to develop a specific gene signature on the TIA-GEP panel to predict CD8-IHC. The correlation between TIA-GEP and CD8-IHC and the prevalence of inflammation were explored across multiple tumor types. Methods: Levels of inflammation were measured by CD8-IHC and TIA-GEP on 1778 procured samples across 12 tumor types. Quality control metrics involved sample input quality, technical errors, and inter-run variability. Generalized linear models were used to identify an inflammation score that predicts the CD8-IHC score in melanoma and SCCHN tissue. The predictive accuracy of this signature was also examined in 10 additional tumor types. Results: Assessment of TME inflammation by CD8-IHC was consistent with that observed by TIA-GEP in multiple tumor types. The range of inflammation varied across different tumor types, with relatively lower inflammation range and scores in SCLC, ovarian, and prostate cancers, and higher values in NSCLC, melanoma, SCCHN, and gastric cancers. R2 x 100 values reflecting percent variation in CD8-IHC associated with TIA-GEP ranged from 62.4% to 79.2% ( P < 0.0001) for all tumor types except prostate cancer (32.5%). Low correlation in prostate cancer may be a result of low prevalence of inflammation by CD8-IHC. Estimated linear regression slopes between CD8-IHC and TIA-GEP ranged from 0.74 in SCLC to 1.27 in gastric cancer. Conclusions: The results suggest that the inflammation signature is a robust potential diagnostic tool predicting inflammation in the TME. The inflammation signature not only correlates with CD8-IHC for multiple tumor types, but also leverages the alternative benefits associated with TIA-GEP, which include information related to tumor inflammation-associated biomarkers and flexibility in exploring the value of other genomic signatures.

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Fischer-Fodor, Eva, Natalia Miklasova, Ioana Berindan-Neagoe, and Bhaskar Saha. "IRON, INFLAMMATION AND INVASION OF CANCER CELLS." Medicine and Pharmacy Reports 88, no. 3 (July 22, 2015): 272–77. http://dx.doi.org/10.15386/cjmed-492.

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Chronic inflammation is associated with the metastasis of tumor cells evolving from a benign tumor to disseminating cancer. Such a metastatic progression is fostered by the angiogenesis propelled by various mediators interacting at the site of tumor growth. Angiogenesis causes two major changes that are assisted by altered glycosylation and neo-antigen presentation by the cancer cells. The angiogenesis-promoted pathological changes include enhanced inflammation and degradation of tissue matrices releasing tumor cells from the site of its origin. The degraded tumor cells release the neo-antigens resulting from altered glycosylation. Presentation of neo-antigens to T cells escalates metastasis and inflammation. Inflammasome activation and inflammation in several infections are regulated by iron. Based on the discrete reports, we propose a link between iron, inflammation, angiogenesis and tumor growth. Knowing the link better may help us formulate a novel strategy for cancer immunotherapy.

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Qian, Shehua, Olga Golubnitschaja, and Xianquan Zhan. "Chronic inflammation: key player and biomarker-set to predict and prevent cancer development and progression based on individualized patient profiles." EPMA Journal 10, no. 4 (November 20, 2019): 365–81. http://dx.doi.org/10.1007/s13167-019-00194-x.

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AbstractA strong relationship exists between tumor and inflammation, which is the hot point in cancer research. Inflammation can promote the occurrence and development of cancer by promoting blood vessel growth, cancer cell proliferation, and tumor invasiveness, negatively regulating immune response, and changing the efficacy of certain anti-tumor drugs. It has been demonstrated that there are a large number of inflammatory factors and inflammatory cells in the tumor microenvironment, and tumor-promoting immunity and anti-tumor immunity exist simultaneously in the tumor microenvironment. The typical relationship between chronic inflammation and tumor has been presented by the relationships between Helicobacter pylori, chronic gastritis, and gastric cancer; between smoking, development of chronic pneumonia, and lung cancer; and between hepatitis virus (mainly hepatitis virus B and C), development of chronic hepatitis, and liver cancer. The prevention of chronic inflammation is a factor that can prevent cancer, so it effectively inhibits or blocks the occurrence, development, and progression of the chronic inflammation process playing important roles in the prevention of cancer. Monitoring of the causes and inflammatory factors in chronic inflammation processes is a useful way to predict cancer and assess the efficiency of cancer prevention. Chronic inflammation-based biomarkers are useful tools to predict and prevent cancer.

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40

Sekar, Divya, Christina Dillmann, Evelyn Sirait-Fischer, Annika F. Fink, Aleksandra Zivkovic, Natalie Baum, Elisabeth Strack, et al. "Phosphatidylserine Synthase PTDSS1 Shapes the Tumor Lipidome to Maintain Tumor-Promoting Inflammation." Cancer Research 82, no. 8 (February 22, 2022): 1617–32. http://dx.doi.org/10.1158/0008-5472.can-20-3870.

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Abstract An altered lipidome in tumors may affect not only tumor cells themselves but also their microenvironment. In this study, a lipidomics screen reveals increased amounts of phosphatidylserine (PS), particularly ether-PS (ePS), in murine mammary tumors compared with normal tissue. PS was produced by phosphatidylserine synthase 1 (PTDSS1), and depletion of Ptdss1 from tumor cells in mice reduced ePS levels accompanied by stunted tumor growth and decreased tumor-associated macrophage (TAM) abundance. Ptdss1-deficient tumor cells exposed less PS during apoptosis, which was recognized by the PS receptor MERTK. Mammary tumors in macrophage-specific Mertk−/− mice showed similarly suppressed growth and reduced TAM infiltration. Transcriptomic profiles of TAMs from Ptdss1-knockdown tumors and Mertk−/− TAMs revealed that macrophage proliferation was reduced when the Ptdss1/Mertk pathway was targeted. Moreover, PTDSS1 expression correlated positively with TAM abundance but negatively with breast carcinoma patient survival. PTDSS1 thus may be a target to modify tumor-promoting inflammation. Significance: This study shows that inhibiting the production of ether-phosphatidylserine by targeting phosphatidylserine synthase PTDSS1 limits tumor-associated macrophage expansion and breast tumor growth.

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Kong, D., Y.-S. Piao, S. Yamashita, H. Oshima, K. Oguma, S. Fushida, T. Fujimura, et al. "Inflammation-induced repression of tumor suppressor miR-7 in gastric tumor cells." Oncogene 31, no. 35 (December 5, 2011): 3949–60. http://dx.doi.org/10.1038/onc.2011.558.

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Suarez-Lopez, Lucia, Ganapathy Sriram, Yi Wen Kong, Sandra Morandell, Karl A. Merrick, Yuliana Hernandez, Kevin M. Haigis, and Michael B. Yaffe. "MK2 contributes to tumor progression by promoting M2 macrophage polarization and tumor angiogenesis." Proceedings of the National Academy of Sciences 115, no. 18 (April 16, 2018): E4236—E4244. http://dx.doi.org/10.1073/pnas.1722020115.

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Chronic inflammation is a major risk factor for colorectal cancer. The p38/MAPKAP Kinase 2 (MK2) kinase axis controls the synthesis of proinflammatory cytokines that mediate both chronic inflammation and tumor progression. Blockade of this pathway has been previously reported to suppress inflammation and to prevent colorectal tumorigenesis in a mouse model of inflammation-driven colorectal cancer, by mechanisms that are still unclear. Here, using whole-animal and tissue-specific MK2 KO mice, we show that MK2 activity in the myeloid compartment promotes tumor progression by supporting tumor neoangiogenesis in vivo. Mechanistically, we demonstrate that MK2 promotes polarization of tumor-associated macrophages into protumorigenic, proangiogenic M2-like macrophages. We further confirmed our results in human cell lines, where MK2 chemical inhibition in macrophages impairs M2 polarization and M2 macrophage-induced angiogenesis. Together, this study provides a molecular and cellular mechanism for the protumorigenic function of MK2.

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Iyengar, Neil M., Ayca Gucalp, Andrew J. Dannenberg, and Clifford A. Hudis. "Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation." Journal of Clinical Oncology 34, no. 35 (December 10, 2016): 4270–76. http://dx.doi.org/10.1200/jco.2016.67.4283.

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Purpose There is growing evidence that inflammation is a central and reversible mechanism through which obesity promotes cancer risk and progression. Methods We review recent findings regarding obesity-associated alterations in the microenvironment and the local and systemic mechanisms through which these changes support tumor growth. Results Locally, hyperadiposity is associated with altered adipose tissue function, adipocyte death, and chronic low-grade inflammation. Most individuals who are obese harbor inflamed adipose tissue, which resembles chronically injured tissue, with immune cell infiltration and remodeling. Within this distinctly altered local environment, several pathophysiologic changes are found that may promote breast and other cancers. Consistently, adipose tissue inflammation is associated with a worse prognosis in patients with breast and tongue cancers. Systemically, the metabolic syndrome, including dyslipidemia and insulin resistance, occurs in the setting of adipose inflammation and operates in concert with local mechanisms to sustain the inflamed microenvironment and promote tumor growth. Importantly, adipose inflammation and its protumor consequences can be found in some individuals who are not considered to be obese or overweight by body mass index. Conclusion The tumor-promoting effects of obesity occur at the local level via adipose inflammation and associated alterations in the microenvironment, as well as systemically via circulating metabolic and inflammatory mediators associated with adipose inflammation. Accurately characterizing the obese state and identifying patients at increased risk for cancer development and progression will likely require more precise assessments than body mass index alone. Biomarkers of adipose tissue inflammation would help to identify high-risk populations. Moreover, adipose inflammation is a reversible process and represents a novel therapeutic target that warrants further study to break the obesity-cancer link.

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Digifico, Elisabeth, Silvia Balinzo, and Cristina Belgiovine. "The Dark Side of the Force: When the Immune System Is the Fuel of Tumor Onset." International Journal of Molecular Sciences 22, no. 3 (January 27, 2021): 1224. http://dx.doi.org/10.3390/ijms22031224.

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Nowadays, it is well accepted that inflammation is a critical player in cancer, being, in most cases, the main character of the process. Different types of tumor arise from sites of infection or chronic inflammation. This non-resolving inflammation is responsible for tumor development at different levels: it promotes tumor initiation, as well as tumor progression, stimulating both tumor growth and metastasis. Environmental factors, lifestyle and infections are the three main triggers of chronic immune activation that promote or increase the risk of many different cancers. In this review, we focus our attention on tumor onset; in particular, we summarize the knowledge about the cause and the mechanisms behind the inflammation-driven cancer development.

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Muñoz-Pérez, Víctor M., Raquel Cariño-Cortés, Iris C. López-Santillán, and Andrés Salas-Casas. "Inflammation in Cancer Development." Mexican Journal of Medical Research ICSA 10, no. 19 (January 5, 2022): 48–51. http://dx.doi.org/10.29057/mjmr.v10i19.8112.

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Inflammation plays an important role to the development of cancer and promotes all stages of tumorigenesis. Cancer cells, as well as inflammatory cells, carry out reciprocal interactions to form an inflammatory tumor microenvironment (TME). Cancer cells within the TME are highly able to change their phenotypic and functional characteristics. Here, we review the relationship between inflammation and infection in cancer origins, and the mechanisms whereby inflammation and infection drive tumor formation. We discuss how infection promotes tumorigenesis related to inflammatory processes typically found in autoimmune diseases, release of inflammatory mediators induced by tumors, inflammation induced by therapy in cancer, and stimuli for induction of inflammation during tumorigenesis, including spatiotemporal considerations. A better understanding of the fundamental rules of engagement that govern the molecular and cellular mechanisms of tumor-promoting inflammation will be essential for further development of cancer therapies.

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Xu, Hui, Donggou He, Hui Li, Nabiha Yusuf, Craig Elmets, Mohammad Athar, Santosh Katiyar, and John Mountz. "IL-17 promotes inflammation associated tumor development (100.14)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 100.14. http://dx.doi.org/10.4049/jimmunol.184.supp.100.14.

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Abstract The mechanism for inflammation associated tumor development is a central issue for tumor biology and immunology. IL-17 is an important cytokine for inflammatory and autoimmune diseases. Although IL-17 producing cells are detected in cancer patients and tumor bearing mice, the role of IL-17 mediated inflammation in tumor development remains to be determined. In the current studies, we showed that IL-17 receptor-A gene deficient mice (IL-17R-/-) were resistant to chemical induced carcinogenesis in the skin. Moreover, the defect in IL-17R reversed the increased susceptibility of IL-12p35 deficient mice to tumor development. Analysis showed that angiogenesis and infiltration of myeloid cells were inhibited whereas the infiltration of CD8 T cells was increased in the inflamed skin of IL-17R-/- mice. The development of myeloid derived suppressor cells was inhibited in IL-17R-/- mice. Inflammation induced Cox-2 activity and S100A8/A9 proteins were inhibited and inflammation associated epidermal hyperplasia were suppressed in IL-17R-/- mice. Furthermore, the production of tumor promoting inflammatory cytokines IL-1β and TNF-α were reduced. These findings demonstrate that IL-17 signals are required for inflammation associated tumor development. The study provides insights into a novel mechanism by which IL-17 mediates tumor promoting inflammation and induces tumor escape from immune surveillance. It has major implications for targeting IL-17 in prevention and treatment of tumors.

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Li, Fei, Xufei Du, Fen Lan, Na Li, Chao Zhang, Chen Zhu, Xiaohui Wang, et al. "Eosinophilic inflammation promotes CCL6-dependent metastatic tumor growth." Science Advances 7, no. 22 (May 2021): eabb5943. http://dx.doi.org/10.1126/sciadv.abb5943.

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Compelling evidence suggests that inflammatory components contribute to cancer development. However, eosinophils, involved in several inflammatory diseases, were not fully explored in cancer metastasis. We show that airway inflammatory eosinophilia and colonic inflammation with eosinophil infiltration are both associated with increased metastasis in mice. Eosinophilia is responsible for increased bone metastasis in eosinophil-enriched Cd3δ-Il-5 transgenic (Il-5 Tg) mice. We also observe increased eosinophils in the malignant pleural effusion of cancer patients with pleural metastasis. Mechanistically, eosinophils promote tumor cell migration and metastasis formation through secreting C-C motif chemokine ligand 6 (CCL6). Genetic knockout of Ccl6 in Il-5 Tg mice remarkably attenuates bone metastasis. Moreover, inhibition of C-C chemokine receptor 1 (CCR1, the receptor of CCL6) in tumor cells reduces tumor cell migration and metastasis. Thus, our study identifies a CCL6-dependent prometastatic activity of eosinophils, which can be inhibited by targeting CCR1 and represent an approach to preventing metastatic disease.

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Wu, Xuesong, Tomonori Takekoshi, Ashley Sullivan, and Sam T. Hwang. "Inflammation and Tumor Microenvironment in Lymph Node Metastasis." Cancers 3, no. 1 (March 1, 2011): 927–44. http://dx.doi.org/10.3390/cancers3010927.

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Gebhardt, Christoffer, Astrid Riehl, Moritz Durchdewald, Julia Németh, Gerhard Fürstenberger, Karin Müller-Decker, Alexander Enk, et al. "RAGE signaling sustains inflammation and promotes tumor development." Journal of Experimental Medicine 205, no. 2 (January 21, 2008): 275–85. http://dx.doi.org/10.1084/jem.20070679.

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A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.

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Surace, Laura, Nicole Angelika Scheifinger, Anurag Gupta, and Maries van den Broek. "Radiotherapy supports tumor-specific immunity by acute inflammation." OncoImmunology 5, no. 1 (June 24, 2015): e1060391. http://dx.doi.org/10.1080/2162402x.2015.1060391.

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Journal articles on the topic 'Tumor-inflammation'

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