Academic literature on the topic 'Glioma, microenvironment, tumor associated macrophages'
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Journal articles on the topic "Glioma, microenvironment, tumor associated macrophages"
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Andersen, Johannes K., Hrvoje Miletic, and Jubayer A. Hossain. "Tumor-Associated Macrophages in Gliomas—Basic Insights and Treatment Opportunities." Cancers 14, no. 5 (March 4, 2022): 1319. http://dx.doi.org/10.3390/cancers14051319.
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Glioma refers to a group of primary brain tumors which includes glioblastoma (GBM), astrocytoma and oligodendroglioma as major entities. Among these, GBM is the most frequent and most malignant one. The highly infiltrative nature of gliomas, and their intrinsic intra- and intertumoral heterogeneity, pose challenges towards developing effective treatments. The glioma microenvironment, in addition, is also thought to play a critical role during tumor development and treatment course. Unlike most other solid tumors, the glioma microenvironment is dominated by macrophages and microglia—collectively known as tumor-associated macrophages (TAMs). TAMs, like their homeostatic counterparts, are plastic in nature and can polarize to either pro-inflammatory or immunosuppressive states. Many lines of evidence suggest that immunosuppressive TAMs dominate the glioma microenvironment, which fosters tumor development, contributes to tumor aggressiveness and recurrence and, very importantly, impedes the therapeutic effect of various treatment regimens. However, through the development of new therapeutic strategies, TAMs can potentially be shifted towards a proinflammatory state which is of great therapeutic interest. In this review, we will discuss various aspects of TAMs in the context of glioma. The focus will be on the basic biology of TAMs in the central nervous system (CNS), potential biomarkers, critical evaluation of model systems for studying TAMs and finally, special attention will be given to the potential targeted therapeutic options that involve the TAM compartment in gliomas.
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Tamai, Sho, Toshiya Ichinose, Taishi Tsutsui, Shingo Tanaka, Farida Garaeva, Hemragul Sabit, and Mitsutoshi Nakada. "Tumor Microenvironment in Glioma Invasion." Brain Sciences 12, no. 4 (April 15, 2022): 505. http://dx.doi.org/10.3390/brainsci12040505.
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A major malignant trait of gliomas is their remarkable infiltration capacity. When glioma develops, the tumor cells have already reached the distant part. Therefore, complete removal of the glioma is impossible. Recently, research on the involvement of the tumor microenvironment in glioma invasion has advanced. Local hypoxia triggers cell migration as an environmental factor. The transcription factor hypoxia-inducible factor (HIF) -1α, produced in tumor cells under hypoxia, promotes the transcription of various invasion related molecules. The extracellular matrix surrounding tumors is degraded by proteases secreted by tumor cells and simultaneously replaced by an extracellular matrix that promotes infiltration. Astrocytes and microglia become tumor-associated astrocytes and glioma-associated macrophages/microglia, respectively, in relation to tumor cells. These cells also promote glioma invasion. Interactions between glioma cells actively promote infiltration of each other. Surgery, chemotherapy, and radiation therapy transform the microenvironment, allowing glioma cells to invade. These findings indicate that the tumor microenvironment may be a target for glioma invasion. On the other hand, because the living body actively promotes tumor infiltration in response to the tumor, it is necessary to reconsider whether the invasion itself is friend or foe to the brain.
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Kennedy, Benjamin C., Christopher R. Showers, David E. Anderson, Lisa Anderson, Peter Canoll, Jeffrey N. Bruce, and Richard C. E. Anderson. "Tumor-Associated Macrophages in Glioma: Friend or Foe?" Journal of Oncology 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/486912.
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Tumor-associated macrophages (TAMs) contribute substantially to the tumor mass of gliomas and have been shown to play a major role in the creation of a tumor microenvironment that promotes tumor progression. Shortcomings of attempts at antiglioma immunotherapy may result from a failure to adequately address these effects. Emerging evidence supports an independent categorization of glioma TAMs as alternatively activated M2-type macrophages, in contrast to classically activated proinflammatory M1-type macrophages. These M2-type macrophages exert glioma-supportive effects through reduced anti-tumor functions, increased expression of immunosuppressive mediators, and nonimmune tumor promotion through expression of trophic and invasion-facilitating substances. Much of our work has demonstrated these features of glioma TAMs, and together with the supporting literature will be reviewed here. Additionally, the dynamics of glioma cell-TAM interaction over the course of tumor development remain poorly understood; our efforts to elucidate glioma cell-TAM dynamics are summarized. Finally, the molecular pathways which underlie M2-type TAM polarization and gene expression similarly require further investigation, and may present the most potent targets for immunotherapeutic intervention. Highlighting recent evidence implicating the transcription factor STAT3 in immunosuppressive tumorigenic glioma TAMs, we advocate for gene array-based approaches to identify yet unappreciated expression regulators and effector molecules important to M2-type glioma TAMs polarization and function within the glioma tumor microenvironment.
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Rao, Rohit, Rong Han, Sean Ogurek, Lai Man Wu, Liguo Zhang, Jian Hu, Matthew Garrett, Tim Phoenix, Stephen N. Waggoner, and Qing Richard Lu. "TAMI-31. GLIOBLASTOMA GENETIC DRIVERS DICTATE THE FUNCTION OF TUMOR-ASSOCIATED MACROPHAGES/MICROGLIA AND RESPONSES TO CSF1R INHIBITION." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi204. http://dx.doi.org/10.1093/neuonc/noab196.815.
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Abstract Tumor-associated macrophages/microglia (TAMs) are prominent microenvironment components in human glioblastoma (GBM) that are potential targets for anti-tumor therapy. However, TAM depletion by CSF1R inhibition showed mixed results in clinical trials. We hypothesized that GBM subtype-specific tumor microenvironment convey distinct sensitivities to TAM targeting. We generated syngeneic PDGFB-driven and RAS-driven GBM models that resemble proneural-like and mesenchymal-like gliomas, and determined the effect of TAM targeting by CSF1R inhibitor PLX3397 on glioma growth and progression. We also investigated the co-targeting of TAMs and angiogenesis on PLX3397-resistant RAS-driven GBM. Using single-cell transcriptomic profiling, we further explored differences in tumor microenvironment compositions and functions between the proneural-like and mesenchymal-like glioma models. We found that the growth of PDGFB-driven tumors was markedly inhibited by PLX3397. In contrast, depletion of TAMs at the early phase accelerated RAS-driven tumor growth and had no effects on other proneural and mesenchymal human GBM models. In addition, PLX3397-resistant RAS-driven tumors did not respond to PI3K signaling inhibition. Single-cell transcriptomic profiling revealed that PDGFB-driven gliomas induced expansion and activation of pro-tumor microglia, whereas mesenchymal RAS-driven gliomas elicited TAMs enriched in pro-inflammatory and angiogenic signaling. Co-targeting of TAMs and angiogenesis decreased cell proliferation and tumor mass in RAS-driven gliomas. Our work identifies functionally distinct TAM subpopulations in the growth of different glioma subtypes. Notably, we uncover a potential responsiveness of resistant mesenchymal-like gliomas to combined anti-angiogenic therapy and CSF1R inhibition. These data highlight the importance of microenvironment landscape characterization to optimally stratify glioma patients for TAM-targeted therapy.
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Wang, Qiang-Wei, Li-Hua Sun, Ying Zhang, Zheng Wang, Zheng Zhao, Zhi-Liang Wang, Kuan-Yu Wang, et al. "MET overexpression contributes to STAT4-PD-L1 signaling activation associated with tumor-associated, macrophages-mediated immunosuppression in primary glioblastomas." Journal for ImmunoTherapy of Cancer 9, no. 10 (October 2021): e002451. http://dx.doi.org/10.1136/jitc-2021-002451.
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BackgroundDysregulated receptor tyrosine kinases, such as the mesenchymal-epidermal transition factor (MET), have pivotal role in gliomas. MET and its interaction with the tumor microenvironment have been previously implicated in secondary gliomas. However, the contribution of MET gene to tumor cells’ ability to escape immunosurveillance checkpoints in primary gliomas, especially in glioblastoma (GBM), which is a WHO grade 4 glioma with the worst overall survival, is still poorly understood.MethodsWe investigated the relationship between MET expression and glioma microenvironment by using multiomics data and aimed to understand the potential implications of MET in clinical practice through survival analysis. RNA expression data from a total of 1243 primary glioma samples (WHO grades 2–4) were assembled, incorporating The Cancer Genome Atlas, Chinese Glioma Genome Atlas, and GSE16011 data sets.ResultsPearson’s correlation test from the three data sets indicated that MET showed a robust correlation with programmed death-ligand 1 (PD-L1) and STAT pathways. Western blot analysis revealed that in GBM cell lines (N33 and LN229), PD-L1 and phosphorylated STAT4 were upregulated by MET activation treatment with hepatocyte growth factor and were downregulated on MET suppression by PLB-1001. Tumor tissue microarray analysis indicated a positive correlation between MET and PD-L1 and macrophage-associated markers. Chromatin immunoprecipitation-PCR assay showed enrichment of STAT4 in the PD-L1 DNA. Transwell co-culture and chemotaxis assays revealed that knockdown of MET in GBM cells inhibited macrophage chemotaxis. Moreover, we performed CIBERSORTx and single-cell RNA sequencing data analysis which revealed an elevated number of macrophages in glioma samples with MET overexpression. Kaplan-Meier survival analysis indicated that activation of the MET/STAT4/PD-L1 pathway and upregulation of macrophages were associated with shorter survival time in patients with primary GBM.ConclusionsThese data indicated that the MET-STAT4-PD-L1 axis and tumor-associated macrophages might enforce glioma immune evasion and were associated with poor prognosis in GBM samples, suggesting potential clinical strategies for targeted therapy combined with immunotherapy in patients with primary GBM.
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Peng, Yichen, Feng Chen, Shenglan Li, Xiu Liu, Can Wang, Chunna Yu, and Wenbin Li. "Tumor‐associated macrophages as treatment targets in glioma." Brain Science Advances 6, no. 4 (December 2020): 306–23. http://dx.doi.org/10.26599/bsa.2020.9050015.
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Gliomas, the most common primary tumors in the central nervous system (CNS), can be categorized into 4 grades according to the World Health Organization. The most malignant glioma type is grade Ⅳ, also named glioblastoma multiforme (GBM). However, the standard treatment of concurrent temozolomide (TMZ) chemotherapy and radiotherapy after maximum resection does not improve overall survival in patients with GBM. Targeting components of the CNS microenvironment represents a new strategy for improving the efficacy of glioma treatment. Most recent studies focused on T cells. However, there is a growing body of evidence that tumor‐associated macrophages (TAMs) play an important role in tumor progression and can be regulated by a wide array of cytokines or chemokines. New TAM‐associated immunotherapies may improve clinical outcomes by blocking tumor progression and prolonging survival. However, understanding the exact roles and possible mechanisms of TAMs in the tumor environment is necessary for developing this promising therapeutic target and identifying potential diagnostic markers for improved prognosis. This review summarizes the possible interactions between TAMs and glioma progression and discusses the potential therapeutic directions for TAM‐associated immunotherapies.
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Jang, Bum-Sup, and In Ah Kim. "Relationship between Macrophage and Radiosensitivity in Human Primary and Recurrent Glioblastoma: In Silico Analysis with Publicly Available Datasets." Biomedicines 10, no. 2 (January 27, 2022): 292. http://dx.doi.org/10.3390/biomedicines10020292.
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The glioblastoma microenvironment predominantly contains tumor-associated macrophages that support tumor growth and invasion. We investigated the relationship between tumor radiosensitivity and infiltrating M1/M2 macrophage profiles in public datasets of primary and recurrent glioblastoma. We estimated the radiosensitivity index (RSI) score based on gene expression rankings. Macrophages were profiled using the deconvolution algorithm CIBERSORTx. Samples from The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), the Ivy Glioblastoma Atlas Project dataset, a single-cell RNA sequencing dataset (GSE84465), Glioma Longitudinal Analysis Consortium (GLASS), and an immunotherapy trial dataset (GSE121810) were included. RSI-high radioresistant tumors were associated with worse overall survival in TCGA and CGGA than RSI-low tumors. M1/M2 macrophage ratios and RSI scores were inversely associated, indicating that radioresistant glioblastoma tumor microenvironments contain more M2 than M1 macrophages. In the single-cell RNA sequencing dataset, the mean RSI of neoplastic cells was positively correlated with high M2 macrophages proportions. A favorable response to programmed cell death protein 1 (PD-1) therapy was observed in recurrent glioblastomas with high M1/M2 macrophage ratios and low RSI scores. In patients with recurrent glioblastoma, fewer M2 macrophages and low RSI scores were associated with improved overall survival. High M2 macrophage proportions may be involved in radioresistant glioblastoma.
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Kim, In Ah, and Bum Sup Jang. "TMIC-52. RELATIONSHIP BETWEEN MACROPHAGE AND RADIOSENSITIVITY IN HUMAN PRIMARY AND RECURRENT GLIOBLASTOMA: IN SILICO ANALYSIS WITH PUBLICLY AVAILABLE DATASETS." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii283. http://dx.doi.org/10.1093/neuonc/noac209.1096.
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Abstract The glioblastoma microenvironment predominantly contains tumor-associated macrophages that support tumor growth and invasion. We investigated the relationship between tumor radiosensitivity and infiltrating M1/M2 macrophage profiles in public datasets of primary and recurrent glioblastoma. We estimated the radiosensitivity index (RSI) score based on gene expression rankings. Macrophages were profiled using the deconvolution algorithm CIBERSORTx. Samples from The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), the Ivy Glioblastoma Atlas Project dataset, a single-cell RNA sequencing dataset (GSE84465), Glioma Longitudinal Analysis Consortium (GLASS), and an immunotherapy trial dataset (GSE121810) were included. RSI-high radioresistant tumors were associated with worse overall survival in TCGA and CGGA than RSI-low tumors. M1/M2 macrophage ratios and RSI scores were inversely associated, indicating that radioresistant glioblastoma tumor microenvironments contain more M2 than M1 macrophages. In the single-cell RNA sequencing dataset, the mean RSI of neoplastic cells was positively correlated with high M2 macrophages proportions. A favorable response to programmed cell death protein 1 (PD-1) therapy was observed in recurrent glioblastomas with high M1/M2 macrophage ratios and low RSI scores. In patients with recurrent glioblastoma, fewer M2 macrophages and low RSI scores were associated with improved overall survival. High M2 macrophage proportions may be involved in radioresistant glioblastoma.
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Richard, Seidu A. "The Pivotal Immunoregulatory Functions of Microglia and Macrophages in Glioma Pathogenesis and Therapy." Journal of Oncology 2022 (April 4, 2022): 1–19. http://dx.doi.org/10.1155/2022/8903482.
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Gliomas are mixed solid tumors composed of both neoplastic and nonneoplastic cells. In glioma microenvironment, the most common nonneoplastic and infiltrating cells are macrophages and microglia. Microglia are the exact phagocytes of the central nervous system, whereas macrophages are myeloid immune cells that are depicted with ardent phagocytosis. Microglia are heterogeneously located in almost all nonoverlapping sections of the brain as well as the spinal cord, while macrophages are derived from circulating monocytes. Microglia and macrophages utilize a variety of receptors for the detection of molecules, particles, and cells that they engulf. Both microglia and peripheral macrophages interact directly with vessels both in the periphery of and within the tumor. In glioma milieu, normal human astrocytes, glioma cells, and microglia all exhibited the ability of phagocytosing glioma cells and precisely apoptotic tumor cells. Also, microglia and macrophages are robustly triggered by the glioma via the expression of chemoattractants such as monocyte chemoattractant protein, stromal-derived factor-1, and macrophage-colony stimulating factor. Glioma-associated microglia and/or macrophages positively correlated with glioma invasiveness, immunosuppression, and patients’ poor outcome, making these cells a suitable target for immunotherapeutic schemes.
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Wei, Jun, Konrad Gabrusiewicz, and Amy Heimberger. "The Controversial Role of Microglia in Malignant Gliomas." Clinical and Developmental Immunology 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/285246.
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Malignant gliomas contain stroma and a variety of immune cells including abundant activated microglia/macrophages. Mounting evidence indicates that the glioma microenvironment converts the glioma-associated microglia/macrophages (GAMs) into glioma-supportive, immunosuppressive cells; however, GAMs can retain intrinsic anti-tumor properties. Here, we review and discuss this duality and the potential therapeutic strategies that may inhibit their glioma-supportive and propagating functions.
Dissertations / Theses on the topic "Glioma, microenvironment, tumor associated macrophages"
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Saavedra, López Elena. "Stimulation of Glioma-Associated Microglia/Macrophages effector phagocytic synapse towards tumor clearance in glioma." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667801.
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Glioblastoma (GBM) es el tumor más agresivo dentro de la clasificación de gliomas y actualmente no tiene cura. Dado que hasta el 30% de las células en GBM son microglia y macrófagos (GAMMs desde ahora, por sus siglas en ingles), decidimos estudiarlos para ayudar en el diseño de posibles futuras inmunoterapias.
El primer gran descubrimiento de esta tesis es la presencia de GAMM en las pseudo-empalizadas (PPs, por sus siglas en inglés) in GBM humano. Estas estructuras se cree que pueden contribuir a la capacidad de invasión del tumor, por lo que el papel de los GAMM en este microambiente puede ser crucial. En concreto, describimos que los GAMMs viajan a través de las PPs hacia su foco necrótico, de forma inversa a las células tumorales. Además, los GAMMs parece que ganan persistencia celular, es decir que viajan de forma directa, bajo las condiciones hipóxicas de las PPs y se desplazan de manera haptotáctica, siendo las fibras GFAP+ su sustrato para avanzar. Al llegar al área necrótica, cambian su fenotipo y fagocitan material del tumor, incluyendo fragmentos GFAP+ y núcleos celulares.
En segundo lugar, en cultivos celulares hemos inducido la translocación de NF-κB p65 para aumentar la facogitosis de células de glioma (C6) por parte de microglia primaria de rata. Además, por medio de líneas celulares inmortalizadas (BV-2 y GL261) hemos descrito una serie de supuestos pasos que pueden ser importantes en el proceso de fagocitosis, así como la distribución de determinados receptores (CD11b y CD16/32) durante estas etapas. Asimismo, describimos la distribución de Iba-1 en los procesos de interacción fagocítica en modelos animales de glioma.
Por último, hemos probado dos estrategias de inmunoterapia en un modelo murino de GBM (ratones C57/BL6 inyectados con células GL261 intracranealmente), descubriendo que estas inmunoterapias tienen efectos distintos: mientras la neutralización de CD47 pareció no ser efectiva, neutralizar SIRP1α parece ser beneficiosa. Así, los animales del grupo denominado CD47 no mostraban un aumento de su supervivencia comparados con los ratones control, incluso mostraban pérdida de peso, indicador de que la terapia pueda producir efectos secundarios sistémicos. Por otro lado, el bloqueo de SIRP permitió el incremento del peso corporal de los animales durante el experimento, y, de hecho, disminuyó el número de células en el centro del tumor incrementando la capacidad fagocítica de los GAMMs en las zonas periféricas de invasión, sin interferir en su capacidad de infiltrar en el tumor.
En conclusión, esta tesis contribuye a una mejor comprensión de la función de los GAMMs en GBM y su capacidad fagocítica intrínseca, posiblemente ayudando al desarrollo de nuevas herramientas terapéuticas para luchar contra este tumor.Glioblastoma (GBM) is the most aggressive form of glioma and currently has no cure. Given that around 30% of the cells within the tumor are microglia/macrophages (glioma- associated microglia/macrophages or GAMM from now on), we decided to study them in order to shed light in possible future immunotherapies. The first discovery during this investigation was the presence of GAMM in pseudopalisades (PPs) of human GBM. These structures are thought to be very important in the contribution of the tumor invasiveness, therefore the knowledge of the role of GAMMs here might be crucial. Particularly, GAMMs were found to be traveling through the PPs towards the necrotic focus, contrasting with the tumor cells. Moreover, the myeloid cells seem to gain cellular persistence with the hypoxic gradient and travel in a haptotactic manner using the gradient of glioma cells as a cue. When they reach the necrotic focus, they shift their phenotype and phagocytose tumor material, including GFAP+ fragments and nuclei. Secondly, by means of cell cultures we achieved to translocate p65 NF-κB and promote phagocytosis of tumor glioma cells (C6) by primary microglia. Moreover, using cell lines (BV-2 and GL261) we described the putative steps of phagocytosis and the distribution of some receptors (CD11b and CD16/32) involved in the process of phagocytosis. Importantly, the distribution of Iba-1 in interacting GAMMs was also defined in the animal models. Finally, we tested two immunotherapy strategies in a immunocompetent GBM animal model (C57/BL6 intracraneally inoculated with GL261 cells), and discovered that both immunotherapies have different outcomes: while CD47 neutralizing antibody seemed to be non-effective, neutralizing SIRP1α had a beneficial outcome. This way, anti-CD47 treated animals did not have any increase on survival rate than control groups; and they showed decreased bodyweight throughout the experiment, suggesting that the therapy had some systemic side effects. On the other hand, blocking SIRP1α allowed the increase of the bodyweight of the animals throughout the experiment, and decreased the cellularity of the tumor core by increasing the phagocytic activity of GAMM at the peripheral area of tumor invasion without interfering in their infiltration capacity. In all, this thesis contributes to a better understanding of the role of GAMMs in GBM and the intrinsic phagocytic capacity they can play, possibly helping in the development of immunotherapeutic tools to fight this fatal tumor.
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Halin, Sofia. "Targeting the prostate tumor microenvironment and vasculature : the role of castration, tumor-associated macrophages and pigment epithelium-derived factor." Doctoral thesis, Umeå universitet, Patologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-30300.
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BACKGROUND: Prostate cancer is the most common cancer among Swedish men. For patients with metastatic prostate cancer the standard therapy is castration, a treatment that initially provides symptomatic relief but unfortunately is not curative. New therapeutic targets for advanced prostate cancer are therefore needed. Prostate cancers are composed of tumor epithelial cells as well as many non-epithelial cells such as cancer associated fibroblasts, blood vessels and inflammatory cells. Many components of the tumor microenvironment such as tumor associated macrophages and angiogenesis have been shown to stimulate tumor progression. This thesis aims to explore mechanisms by which the local environment influences prostate tumor growth and how such mechanisms could be targeted for treatment. MATERIALS AND METHODS: We have used animal models of prostate cancer, in vitro cell culture systems and clinical materials from untreated prostate cancer patients with long follow up. Experiments were evaluated with stereological techniques, immunohistochemistry, western blotting, quantitative real-time PCR, PCR arrays and laser micro dissection. RESULTS: We found that the presence of a tumor induces adaptive changes in the surrounding non-malignant prostate tissue, and that androgen receptor negative prostate tumor cells respond to castration treatment with temporarily reduced growth when surrounded by normal castration-responsive prostate tissue. Further, we show that macrophages are important for prostate tumor growth and angiogenesis in the tumor and in the surrounding non-malignant tissue. In addition, the angiogenesis inhibitor Pigment epithelium-derived factor (PEDF) was found to be down-regulated in metastatic rat and human prostate tumors. Over-expression of PEDF inhibited experimental prostate tumor growth, angiogenesis and metastatic growth and stimulated macrophage tumor infiltration and lymphangiogenesis. PEDF was found to be down-regulated by the prostate microenvironment and tumor necrosis factor (TNF) α. CONCLUSIONS: Our studies indicate that not only the nearby tumor microenvironment but also the surrounding non-malignant prostate tissue are important for prostate tumor growth. Both the tumor and the surrounding non-malignant prostate were characterized by increased angiogenesis and inflammatory cell infiltration. Targeting the surrounding prostate tissue with castration, targeting tumor associated macrophages, or targeting the vasculature directly using inhibitors like PEDF were all shown to repress prostate tumor growth and could prove beneficial for patients with advanced prostate cancer.
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Gurusamy, Devikala. "Epithelial and Stromal Ron Receptor Expression Promotes Tumor Growth in a Murine Model of Prostate Cancer." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367929231.
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Eduardo, Rodrigo. "Exploring Tumor Macrophage Interaction in Anaplastic Thyroid Cancer." Master's thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica António Xavier, 2019. http://hdl.handle.net/10362/130111.
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"Anaplastic thyroid cancer (ATC) is the most aggressive form of thyroid cancer, with very high mortality rate. Tumor-associated macrophages (TAMs) can represent up to 70% of ATC’s tumor mass, making them an interesting target for novel therapies.
In this thesis, the aim was to further understand the crosstalk between ATC and TAMs. To achieve that, cell surface proteomics of two ATC cell lines (C3948 and T235), in mono- or co-culture with THP-1-derived macrophage-like cells, was performed. The protein Spry-4, an inhibitor of the MAPK-ERK pathway, was found to be downregulated in C3948 cells upon co-culture. Spry-4 protein levels were further evaluated by Western blot; only T235 in co-culture showed a trend for downregulation, although without statistical significance.(...)"N/A
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Mola, Silvia. "Tumor Associated Macrophages (TAMs) a pivotal orchestrator in cancer-related inflammation and a new important target in cancer-therapy." Doctoral thesis, Università del Piemonte Orientale, 2021. https://hdl.handle.net/11579/127797.
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Macrophages are pivotal orchestrators of tumor-promoting inflammation and promising targets for new anti-cancer therapies. To identify new molecular players underlying their pro-tumoral activities, we analyzed the phosphoproteoma of tumor associated macrophages (TAMs) isolated from murine fibrosarcoma. We identified the protein TRIM28, a pleiotropic molecule that is known to be involved in the dynamic organization of chromatin, and we characterized the signaling pathway driving its phosphorylation in response to inflammatory signals and its impact on LPS-induced gene expression. We explored in vivo the functional relevance of TRIM28 and found a significant reduction of colitis associated cancer lesions in mice lacking TRIM28 in intestinal epithelial cells. Single cell RNAseq analysis pointed out alterations of both immune and intestinal cell populations during the transition from colitis to cancer, that are dependent on TRIM28. Overall, these results identify TRIM28 as a new molecular target at the crossroads between inflammation and cancer.
Beyond contributing to tumorigenesis, TAMs can profoundly affect the response to anti-cancer therapies. We investigated their impact on EPZ-6438, an inhibitor of the histone methyltransferase EZH2 that has recently entered in clinical trials due to the anti-proliferative effects shown on malignant pleural mesothelioma cells (MPM). We generated an MPM spheroid model that recapitulates in vitro, both monocyte recruitment in tumor and their functional differentiation towards a TAM-like phenotype (Mo-TAMs) capable of promoting tumor cell proliferation and spreading. Prolonged treatment of MPM spheroids with EPZ-6438 enhances both Mo-TAMs recruitment and pro-tumor phenotype expression, thereby limiting the anti-proliferative effects due to EZH2 inhibition in MPM cells. These findings indicate that strategies of TAM depletion should be combined with EPZ-6438 to improve the therapeutic efficacy of pharmacological EZH2 inhibition.
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FERRUCCI, VERONICA. "PRUNE-1 DRIVES THE RECRUITMENT AND THE POLARIZATION OF TUMOUR-ASSOCIATED MACROPHAGES (TAMS) PREPARING THE SOIL FOR LUNG METASTASES IN TRIPLE NEGATIVE BREAST CANCER." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/563230.
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Tumour microenvironment is a complex network of cells, including immune cells, with a role in tumorigenesis and metastatic spread. Among the immune cells, M2-polarized Tumour-Associated-Macrophages (M2-TAMs) show immunosuppressive activities by expressing inflammatory molecules, thus promoting tumorigenesis. Triple-Negative Breast Cancer (TNBC), lacking both hormone receptors (i.e. Progesterone Receptor [PgR] and Estrogen Receptor [ER]) and Human Epidermal growth factor Receptor 2 (HER2), is associated with poor prognosis and high probability of distant metastases. In TNBC, a large number of infiltrating M2-TAMs is positively correlated to higher risk of metastases and lower rates of Disease-Free Survival” (EFS) and Overall Survival (OS).
Prune-1 belongs to DHH (Asp-His-His) phosphoesterase superfamily with an exopolyphosphatase activity. The overexpression of Prune-1 is correlated with metastases and poor prognosis in several tumours including Breast Cancer (BC). Prune-1 was also found to induce Epithelial-Mesenchimal-Transition (EMT) and metastatic dissemination throught the enhancement of canonical TGF-β signaling by counterbalancing its inhibition operated by NDPK-A. Further evidences suggested that lung cancer progression is driven by Prune-1 through the canonical WNT signaling pathway in both autocrine and paracrine manner via Wnt3a cytokine secretion, thus suggesting a potential role for Prune-1 also in extracellular environment.
Here, we identified Prune-1 protein as overexpressed in TNBC patients and positively correlated to lynphnode metastases, inflammatory pathways and infiltrating M2-TAMs (CD68+/CD163+).
Furthermore, we developed a Genetically Engineered Mouse Model (GEMM) of metastatic TNBC over-expressing both Prune-1 and Wnt-1 in mammary glands (MMTV-Prune1/Wnt1). We found Prune-1 to recruit TAMs and to enhance their polarization toward a pro-tumorigenic M2-phenotype in the tumour microenvironment, thus promoting lung metastases in this GEMM. We also show that Prune-1 takes part to the communication between TNBC cells and TAMs through intracellular pathways activation (i.e., TGF-b and NF-kB), but also in a paracrine manner by inducing the secretion of inflammatory cytokines (e.g., IL-17F and IL-28) and modulating the exosome protein contents.
Finally, we found an anti-Prune-1 drug (AA7.1) with the ability to reduce the primary tumour growth by reducing the percentage of M2-TAMs in orthotopic xenograft immunocompetent models of TNBC.
In conclusion, our GEMM of metastatic TNBC driven by Prune-1 will be a useful source for future immunotherapy pre-clinical trials targeting M2-polarized TAMs within the tumour microenvironment to inhibit distant metastases in TNBC with poor prognosis.
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Alves, Alessandro Menna. "Carcinoma espinocelular de boca e inflamação : papel dos macrófagos no prognóstico e influência de citocinas inflamatórias no comportamento migratório." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/152699.
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O carcinoma espinocelular de boca (CEB) é a neoplasia maligna mais comum da cavidade oral, correspondendo à aproximadamente 94% dos casos dessa região. Apesar dos diversos estudos moleculares e celulares do CEB, a taxa de sobrevida dos pacientes é de aproximadamente 50%, devido principalmente ao tamanho do tumor, metástase em linfonodos regionais, grau de diferenciação das células e sítio anatômico. O microambiente tumoral do CEB, é extremamente complexo e diversificado, tendo como característica principal um estado inflamatório crônico imunossupressivo. Este microambiente é sustentado pela liberação de diferentes citocinas inflamatórias, como IL-6, TNF- - atividades exercidas tanto pelas células tumorais quanto pelas estromais. Dentre essas atividades, tem sido relatado na literatura que as citocinas inflamatórias são capazes de aumentar a migração e a capacidade de invasão das células tumorais. Entre as células estromais, os macrófagos são as mais abundantes e participam da manutenção do microambiente tumoral. De acordo com o estímulo, podem ser polarizados M1, com papel pró-inflamatório e antitumoral, e M2, com papel anti-inflamatório e pró-tumoral. O objetivo desta tese foi compreender o papel dos macrófagos no prognóstico de CEB e das citocinas inflamatórias IL-6, TNF- - linhagens celulares de CEB. Para verificar o papel dos macrófagos no prognóstico, foi realizada uma revisão sistemática na qual foram incluídos apenas os estudos que utilizavam amostra de pacientes com CEB e avaliavam o prognóstico com marcadores para macrófagos. Foi observado que maiores concentrações de macrófagos CD68+ e CD163+ estavam relacionados com pior prognóstico de pacientes com CEB, embora não tenha sido possível concluir qual região tumoral a presença destas células seja mais importante 7 para o desfecho. Para analisar o papel das citocinas inflamatórias IL-6, TNFILensaios in vitro utilizando duas linhagens celulares, SCC25 e Cal27, em condições promotoras de migração sob a influência dessas citocinas. Foi observado que a citocina IL-6 foi capaz de aumentar a velocidade de migração e a direcionalidade tanto da SCC25 quanto da Cal 27 e que esta melhora na capacidade migratória ocorreu através de um crosstalk entre a via de sinalização relacionada a IL6 (STAT3) e a via reguladora de migração celular, Rho GTPase Rac1. Estes dados reforçam o papel do microambiente tumoral no processo de progressão tumoral e sugerem potenciais alvos terapêuticos como a modulação do perfil da população de macrófagos e o papel de interleucinas no controle de invasão tecidual e metástase.Oral squamous cell carcinoma (OSCC) is the most common malignant neoplasm of the oral cavity, corresponding to approximately 94% of the cases in this region. Despite the diverse molecular and cellular studies of OSCC, the patient survival rate is approximately 50%, mainly due to tumor size, regional lymph node metastasis, cell differentiation and anatomic site. The OSCC tumor microenvironment is extremely complex and diverse, with the main characteristic being an immunosuppressive chronic inflammatory state. This microenvironment is supported by the release of different inflammatory cytokines, such as IL-6, TNF- - and enhance the activities of both tumor and stromal cells. Among these activities, it has been reported in the literature that inflammatory cytokines are capable of increasing migration and invasiveness of tumor cells. Among stromal cells, macrophages are the most abundant and participate in the maintenance of the tumor microenvironment. According to the stimulus, macrophages can be polarized in M1, with pro-inflammatory and anti-tumoral role, and M2, with antiinflammatory and pro-tumoral role. Thus, the aim of this thesis was to evaluate the role of macrophages in the prognosis of OSCC and the influence of inflammatory cytokines IL-6, TNF- - OSCC cell lines. To assess the role of macrophages in the prognosis, a systematic review was conducted in which only studies using a sample of OSCC patients were evaluated and the prognosis was evaluated with macrophage markers. It was observed that higher concentrations of CD68 + and CD163 + macrophages were related to worse prognosis in patients with OSCC, although it was not possible to conclude which tumor region the presence of these cells is more important for the outcome. In order to analyze the role of the inflammatory cytokines IL-6, TNF- - atory 9 behavior of OSCC cells, in vitro assays using two cell lines, SCC25 and Cal27, were performed in migration-promoting conditions under the influence of these cytokines. It was observed that IL-6 was able to increase the speed migration and directionality of both SCC25 and Cal 27 and that this improvement in migratory capacity occurred through a crosstalk between the IL6-related signaling pathway (STAT3) and cell migration-related pathway, RhoGTPase Rac1. These data reinforce the role of the tumor microenvironment in the tumor progression process and suggest potential therapeutic targets such as the modulation of the profile of the macrophages population and the role of interleukins in the control of tissue invasion and metastasis.
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Mota, José Mauricio Segundo Correia. "Progressão tumoral de melanoma B16 em camundongos sobreviventes à sepse. Possível papel de macrófagos associados ao tumor através da via CXCR4/CXCL12." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-19072016-165003/.
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Introdução: Indivíduos sobreviventes à sepse apresentam maior mortalidade à longo prazo e maior risco de apresentar infecções oportunistas. Existem evidências clínicas e experimentais de desregulação imune no estado pós-sepse. Essas alterações apresentam semelhança com aquelas encontradas no microambiente tumoral, estando relacionadas à imunossupressão. O presente trabalho avaliou o papel de macrófagos associados ao tumor (TAM) em modelo de progressão tumoral em camundongos sobreviventes à sepse. Materiais e Métodos: Camundongos C57/BL6 foram submetidos a ligadura e punção cecal (CLP) e tratados com ertapenem (20 mg/kg, i.p., 6 horas após CLP e 12/12 h por 3 dias). Os animais sobreviventes de sepse eram inoculados com células de melanoma B16-F10 (30 mil, s.c., 15 dias após a CLP). Animais naïve foram usados como controle. Foram avaliadas a progressão tumoral, sobrevida e formação de metástases espontâneas à distância. No D+14, animais foram sacrificados para mensuração do acúmulo de TAM por citometria de fluxo (CD45+F4/80+CD206+) e de citocinas no soro e no tumor por ELISA (IFN-?, IL-10, TNF-?, TGF-?, CCL2, CXCL12). Macrófagos derivados de medula óssea de animais pós-CLP ou naïve foram coinoculados com células B16 para avaliação de progressão tumoral e sobrevida. TAM de animais naïve ou pós-CLP foram isolados através de gradiente de Percoll seguido de adesão seletiva e o RNA foi isolado para análise diferencial de expressão gênica por microarray. Para avaliação da participação da via CXCL12/CXCR4 foi realizada sua inibição com o AMD3100, antagonista de CXCR4 (5 mg/kg, i.p., D+10 e D+14). Foi avaliada a progressão tumoral, sobrevida, acúmulo de TAM e proliferação extramedular de TAM no D+14. Resultados: Animais sobreviventes de sepse apresentaram aumento de progressão tumoral (após 15, 30 e 60 dias da CLP), aumento da carga de metástases (após 15 dias da CLP) e redução de sobrevida. Foi detectado o aumento de TAM nos animais pós-CLP, associado a maior marcação de Ki67, em comparação com animais naïve no D+14. Verificamos aumento das concentrações séricas de TGF-?, CXCL12, CCL2 e TNF-?. Camundongos naïve que coinoculados com macrófagos derivados de medula óssea de animais pós-CLP apresentaram aumento de progressão tumoral e redução de sobrevida em comparação com o grupo controle. TAM de animais pós-CLP apresentaram menor expressão de genes relacionados ao MHC-II e genes relacionados à ativação leucocitária. A inibição de CXCL12/CXCR4 preveniu a progressão tumoral induzida por sepse, com menor acúmulo de TAM e menor presença de TAM Ki67+. Conclusões: O estado pós-sepse promove a progressão tumoral de melanoma B16 em camundongos, o qual foi associado a aumento de 12 TAM. A via CXCL12/CXCR4 participa do processo de acúmulo de TAM nesse modelo experimental.Background: Survivors from sepsis present higher long-term mortality and increased risk of opportunistic infections. There is clinical and experimental evidence for an immunosuppressive immune dysregulation in post-sepsis. These alterations are similar to those found in tumor microenvironment. The present work assessed the role of tumorassociated macrophage (TAM) in a model of tumor progression in sepsis-surviving mice. Materials and Methods: C57/BL6 mice were submitted to cecal ligation and puncture (CLP) and treated with ertapenem (20 mg/kg, ip. - 6 h after CLP and then each 12 h for 3 days). Sepsis surviving mice were inoculated with B16-F10 melanoma cells (30,000, sc., 15 days after CLP). Naïve mice were used as controls. Tumor progression, survival and distant spontaneous metastasis were evaluated. Mice were killed at D+14 for TAM measurement through flow cytometry (CD45+F4/80+CD206+) and for cytokines (IFN-?, IL-10, TNF-?, TGF-?, CCL2, CXCL12) quantification by ELISA. Bone marrow-derived macrophage (BMDM) were isolated and co-inoculated together with B16 melanoma cells for tumor progression and survival evaluation. TAM from naïve or post-sepsis mice were isolated through Percoll gradient (70/30) followed by selective adhesion. The RNA was isolated for gene expression analysis using microarray assay. To evaluate the role of CXCL12/CXCR4, we used the specific antagonist AMD3100 (5 mg/kg, ip., at D+10 and D+14) and assessed tumor progression, survival and TAM accumulation at D+14. Results: Sepsis-surviving mice showed increased tumor progression (15, 30 or 60 days after CLP), higher metastatic burden (15 days after CLP), and less overall survival. TAM were increased in post-sepsis mice at D+14. We found increased serum levels of TGF-?, CXCL12, CCL2 e TNF-?. Naïve mice inoculated with BMDM from post-sepsis and B16 cells showed higher tumoral progression and less survival, when compared to the control group. TAM from post-sepsis showed decreased expression of MHC-II related genes and genes related to leukocyte activation. The inhibition of CXCL12/CXCR4 prevented the post-sepsis-induced tumor progression, with less TAM accumulation and reduced expression of Ki67 in TAM. Conclusions: The post-sepsis state promotes the progression of B16 melanoma in mice, which was associated with an increase in TAM accumulation. CXCL12/CXCR4 mediates TAM accumulation in this experimental model.
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Kostine, Marie. "Defining the immune microenvironment in sarcoma : could immunotherapy be part of the treatment strategy in sarcoma patients ?" Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0387/document.
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La chirurgie est la pierre angulaire du traitement curatif des sarcomes, lorsqu’elle est possible. En revanche, en cas de maladie avancée ou métastatique, les traitements systémiques ont une efficacité assez limitée avec un réel besoin de nouvelles options thérapeutiques. Le récent succès de l’immunothérapie dans les tumeurs épithéliales soulève donc la question de la possibilité d’une telle approche dans les sarcomes, et surtout pour quels sous-types histologiques. L’objectif de ce travail de thèse était d’obtenir des données précliniques en caractérisant le microenvironnement immunitaire au sein de trois types de sarcomes potentiellement candidats à l’immunothérapie, prérequis indispensable avant d’envisager une application clinique : 1) Dans le chondrosarcome, l’expression de PD-L1 a été retrouvée exclusivement dans près de 50% des chondrosarcomes dédifférenciés, et s’associait à une infiltration lymphocytaire T et l’expression des molécules HLA de classe I. Ces données incitent donc à inclure les patients avec ce sous type de chondrosarcome dans des essais cliniques évaluant un traitement anti PD-1/PD-L1. 2) Dans l’ostéosarcome, un infiltrat lymphocytaire T était observé de façon bien plus importante dans les lésions métastatiques que dans lésions primitives ou rechutes locales. De plus, l’expression de PD-L1 était retrouvée dans presque 50% des métastases mais pas ou peu dans la tumeur primitive correspondante, traduisant ici une dynamique d’échappement au système immunitaire lors de la progression de la maladie. Une stratégie ciblée sur les lymphocytes T visant à amplifier et potentialiser cette réponse immune préexistante dans les lésions métastatiques pourrait donc offrir un bénéfice clinique. 3) Dans le léiomyosarcome, les molécules HLA de classe I étaient fortement exprimées et l’expression de PD-L1 retrouvée dans 30% des tumeurs de haut grade, également très infiltrées par des macrophages immunosuppresseurs CD163+. Une importante infiltration de macrophages CD163+ était un marqueur indépendant de mauvais pronostic pour la survie, indiquant l’intérêt de d’une approche ciblée visant les macrophages dans ce type de sarcome, éventuellement en association avec un traitement anti PD-1/PD-L1Local control with adequate surgery is the cornerstone of sarcoma treatment. However, most sarcoma lack effective systemic therapies in case of advanced disease, emphasizing an unmet medical need for new therapeutic targets. The recent success of immunotherapy in epithelial malignancies raises the question whether such therapies, and which ones, would be applicable in sarcomas. As a prerequisite for therapeutic applications, we characterized the immune microenvironment in three sarcoma subtypes potentially candidate to immunotherapy: 1) In chondrosarcoma, PD-L1 expression was exclusively found in nearly 50% of the dedifferentiated subtype, in association with immune-infiltrating cells and HLA class I expression. These data provide rationale for including such patients in clinical trials with PD-1/PD-L1-targeted therapies. 2) In osteosarcoma, we observed a high density of tumor-infiltrating T cells in metastatic lesions compared to primary tumors and local relapses. Furthermore, PD-L1 positivity in almost half of metastases while mainly negative in the associated primary tumors, emphasises the dynamics of an adaptive mechanism of immune escape. Enhancing the preexisting immune response in metastatic lesions using T-cell-based immunotherapy may offer clinical benefit. 3) In leiomyosarcoma, HLA class I molecules were strongly upregulated and PD-L1 expression found in 30% of high-grade tumors, which were also highly infiltrated with CD163+ immunosuppressive macrophages. CD163+ was found to be an independent poor prognostic factor for overall survival, indicating the need for assessing a macrophage-targeted approach in this tumor type, as single agent or in combination with anti PD-1/PD-L1agents
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Elmously, Sherine mohamed Mohamed Kamel. "The role of the tumor microenvironment in cerebral glioma progression." Doctoral thesis, 2016. http://hdl.handle.net/11562/944431.
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sfondo: Il tumore associato macrofagi (TAMs) sono classificati in pro-infiammatorio M1 TAM, e anti-infiammatori M2 TAM. Le cellule staminali glioma (GSC) polarizzano TAM in M2 fenotipo che promuovono la progressione glioma. E voluto studiare l'implicazione della infiltrazione totale e differenziale TAM in gliomi a basso grado (LGG) e in gliomi a alto grado (HGG). Inoltre abbiamo studiato l'effetto di esosomi rilasciati da M1 TAM sul destino delle cellule di glioma. Metodologia: immunoistochimica è stata eseguita su 11 campioni accoppiati ottenuti da casi di progressione da LGG a HGG. iNOS è stato utilizzato come marcatore per M1 e CD163 come marcatore per M2. Negli esperimenti in vitro, abbiamo polarizzato monociti umani U937 in M1 fenotipo, poi abbiamo isolato i esosomi dal mezzo M1 condizionato con centrifugazione e filtrazione. Dopo aver aggiunto esosomi M1 di cellule di glioma U251, abbiamo studiato l'attivazione delle cellule glioma con il saggio MTT e abbiamo studiato l'apoptosi delle cellule glioma con la citofluorimetria. Abbiamo usato annessina V come marcatore di apoptosi precoce e ioduro di propidio come marcatore di ritardo apoptosi. Risultati: immunoistochimica ha mostrato uno squilibrio M1 / M2 con la maggioranza di essere M2 sia LGG e HGG. La M2 infiltrazione superiore, la prima è stata la progressione. Gli esperimenti in vitro hanno rivelato l'effetto antitumorale di exosomes M1 che erano in grado di inibire la proliferazione e di indurre apoptosi precoce e tardiva delle cellule di glioma. Conclusione: i nostri dati confermano il ruolo di M2 TAM nella progressione di glioma ed espostano il ruolo tumoricidale di esosomi M1 contro i gliomiBackground: The tumor associated macrophages (TAMs) are classified into pro-inflammatory M1 TAMs, and anti-inflammatory M2 TAMs. Glioma stem cells (GSCs) polarize TAMs into M2 phenotype which promote glioma progression. We aimed to study the implication of the total and differential TAM infiltration in low grade glioma (LGG) and high grade glioma (HGG). Also we investigated the effect of exosomes released from M1 TAMs on the fate of glioma cells. Methodolgy: Immunohistochemistry was performed on 11 paired specimens obtained from cases progressing from LGG to HGG. iNOS was used as a marker for M1 and CD163 as a marker for M2. In the in-vitro experiments, we polarized human monocytes U937 into M1 phenotype, then we isolated the exosomes from the M1conditioned medium by centrifugation and filtration. After adding M1 exosomes to U251 glioma cells, we studied the glioma cell activation by MTT assay and we studied the glioma cell apoptosis by flow-cytometry. We used Annexin V as a marker of early apoptosis and propidium iodide as a marker of late apoptosis. Results: immunohistochemistry showed an M1/M2 imbalance with the majority being M2 in either LGG and HGG. The higher M2 infiltration, the earlier was the progression. The in-vitro experiments revealed the anti-tumor effect of M1 exosomes which were able to inhibit the proliferation and to induce early and late apoptosis of glioma cells. Conclusion: our data confirmed the role of M2 TAMs in glioma progression and exhibited the tumoricidal role of M1 exosomes against gliomas.
Books on the topic "Glioma, microenvironment, tumor associated macrophages"
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Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny, and Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.
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Ovarian adenocarcinoma is typified by detection at late stages with dissemination of cancer cells into the peritoneal cavity and frequent acquisition of chemoresistance. A number of studies show the importance of the tumor microenvironment and innate immune recognition in tumor progression. Ovarian cancer cells can regulate the composition of their stroma to promote the formation of ascitic fluid rich in cytokines and bioactive lipids such as PGE2, and to stimulate the differentiation of stromal cells into a pro-tumoral phenotype. In response, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, tumor-associated macrophages, and other peritoneal cells can act through direct and indirect mechanisms to regulate tumor growth, chemoresistance via alteration of class III β tubulin, angiogenesis and dissemination. This chapter deciphers the current knowledge about the role of stromal cells, associated secreted factors, and the immune system on tumor progression. This suggests that targeting the microenvironment holds great potential to improve the prognosis of patients with ovarian adenocarcinoma.
Book chapters on the topic "Glioma, microenvironment, tumor associated macrophages"
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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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Anfray, Clément, Aldo Ummarino, Alfonso Calvo, Paola Allavena, and Fernando Torres Andón. "In Vivo Analysis of Tumor-Associated Macrophages in the Tumor Microenvironment." In Methods in Molecular Biology, 93–108. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2914-7_7.
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Mir, Manzoor Ahmad, Abrar Yousuf Mir, and Tabasum Mushtaq. "Role of tumor-associated macrophages in the breast tumor microenvironment." In Role of Tumor Microenvironment in Breast Cancer and Targeted Therapies, 137–69. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-443-18696-7.00003-8.
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Hughes, Russell, and Munitta Muthana. "The tumor microenvironment: The role of tumor-associated macrophages in cancer progression and responses to therapy." In Tumor Immunology and Immunotherapy, 43–62. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199676866.003.0004.
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Tiwari, Meenakshi, Lokendra Kumar Sharma, and Ajit Kumar Saxena. "Potential Role of Cancer Stem Cells in Glioblastoma: A Therapeutic Aspect." In Glioblastoma - Current Evidences [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106332.
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High-grade glioma (HGG) such as glioblastoma multiforme (GBM) is an aggressive brain tumor that is still associated with poor prognosis. With the discovery and advancement in understanding of cancer stem cells (CSC) in glioma, these cells have emerged as seed cells for tumor growth and recurrence and appear as a potential target for therapeutics. Glioma stem cells (GSCs) demonstrate capacity of self-renewal, proliferation, and differentiation into multiple cell types and can contribute to tumor heterogeneity. Their role is established in tumorigenesis, metastasis, chemo- and radio-resistance and appears as a major cause for tumor recurrence. Thus, targeting GSCs by various therapeutics may improve effectiveness of the drugs in use alone or in combination to significantly improve patient survival outcome in GBM cases. In this chapter, we have discussed various mechanisms that drive GSC including signaling pathways and tumor microenvironment. We have also discussed the mechanism behind resistance of GSCs toward therapeutics and the pathways that can be targeted to improve the outcome of the patients.
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Hooda-Nehra, Anupama, Tracey L. Smith, Alejandra I. Ferrer, Fernanda I. Staquicini, Wadih Arap, Renata Pasqualini, and Pranela Rameshwar. "Targeted Regulation and Cellular Imaging of Tumor-Associated Macrophages in Triple-Negative Breast Cancer: From New Mechanistic Insights to Candidate Translational Applications." In Macrophages celebrating 140 years of discovery [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105654.
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The complex interplay between immune cells and tumor cells within the tumor microenvironment (TME) can lead to disease progression. Specifically, signals generated in the TME can cause immunosuppression, promoting angiogenesis and immune evasion, which leads to tumor development. The interplay of M1 and M2 macrophage populations that coincide with these tumor markers is particularly important in the TME. Triple-negative breast cancer (TNBC) often presents as advanced disease, and these tumors are also often bereft of recognized molecular targets that can be found in other subtypes, limiting their therapeutic options. However, tumor-associated macrophages (TAMs) infiltration in TNBC is frequently observed. Moreover, a high density of TAMs, particularly M2 macrophages, is associated with poorer outcomes in various cancers, including TNBC. This provides a strong basis for exploiting TAMs as potential therapeutic targets. Specifically, efforts to increase M2 to M1 repolarization are promising therapeutic approaches in TNBC, and four recent studies wherein divergent approaches to target the M2-rich macrophage population and reverse immune subversion are described. These and similar efforts may yield promising diagnostic or therapeutic options for TNBC, a great clinical need.
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Ponnoor Anto, Nikhil, and Rashmi Mittal. "Evaluating Fate of Emerging Resistance Hitting the Brakes on Conventional Treatment Approach." In Therapeutic Drug Targets and Phytomedicine For Triple Negative Breast Cancer, 99–122. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815079784123010008.
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The tumor microenvironment of TNBC cells was associated with the induction of angiogenesis, proliferation, apoptosis inhibition, immune suppression, and drug resistance. TME creates a niche for the survival and interaction of cancer cells with surrounding cells. TME promoted epithelial to mesenchymal transition, stemness, and chemoresistance and ensured the escape of TNBC cells from the chemotherapeutic and immunological responses. This chapter highlighted the role of cancer stem cells, hypoxia, lysosomal biomass, tumor-associated macrophages, PTEN, PI3K/Akt/mTOR pathway, and ABC transporters in inducing resistance against standard therapeutic regimens. The possible role of miRNA, transcriptional signatures, and tumor-infiltrating lymphocytes as a predictor of chemoresistance was also depicted. The impact of drug repurposing and combinational therapeutic approach to overcome the obstacle of chemoresistance have been underlined in this chapter for the treatment of TNBC.
Conference papers on the topic "Glioma, microenvironment, tumor associated macrophages"
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Guerriero, Jennifer L., and Anthony Letai. "Abstract A17: Modulation of tumor-associated macrophages towards an antitumor phenotype." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a17.
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Rabe, Daniel C., Casey Frankenberger, Russell Bainer, Devipriya Sankarasharma, Kiran Chada, Thomas Krausz, Yoav Gilad, Lev Becker, and Marsha Rich Rosner. "Abstract A01: Metastasis suppressors regulate the tumor microenvironment by blocking recruitment of pro-metastatic tumor-associated macrophages." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-a01.
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Rabe, Daniel C., Casey Frankenberger, Russell Bainer, Devipriya Sankarasharma, Kiran Chada, Thomas Krausz, Yoav Gilad, Lev Becker, and Marsha Rich Rosner. "Abstract PR02: Metastasis suppressors regulate the tumor microenvironment by blocking recruitment of pro-metastatic tumor-associated macrophages." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-pr02.
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Miyauchi, Jeremy T., Danling Chen, Matthew K. Choi, Kenneth Shroyer, David Selwood, and Stella E. Tsirka. "Abstract 4919: Ablation of neuropilin 1 from glioma-associated microglia and macrophages slows tumor progression." 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.am2017-4919.
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Miyauchi, Jeremy T., Danling Chen, Matthew Choi, Jillian Nissen, Kenneth Shroyer, David Selwood, and Stella E. Tsirka. "Abstract A129: Ablation of neuropilin 1 from glioma associated macrophages and microglia slows tumor progression." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a129.
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Zarif, Jelani C., James R. Hernandez, and Kenneth J. Pienta. "Abstract B34: Targeting M2-tumor associated macrophages (M2-TAMs) in prostate cancer." In Abstracts: AACR Special Conference: The Function of Tumor Microenvironment in Cancer Progression; January 7-10, 2016; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-b34.
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Mathsyaraja, Haritha, Katie Thies, David A. Taffany, and Michael C. Ostrowski. "Abstract A27: Micromanaging the microenvironment: The role of microRNA in metastatic mammary tumor-associated macrophages." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a27.
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Kosoff, David, Jiaquan Yu, Jennifer L. Schehr, David J. Beebe, and Joshua M. Lang. "Abstract 4922: Microscale engineering of the tumor microenvironment for therapeutic targeting of tumor-associated macrophages in prostate 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.am2017-4922.
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Low, Pin Yan, Yaw Chyn Lim, Wei Peng Yong, Bok Yan, and Jimmy So. "Abstract C36: Tumor-associated macrophages enhance tumor invasiveness and promote CD4+ T-cell recruitment in Gastric Cancer." In Abstracts: AACR Special Conference: The Function of Tumor Microenvironment in Cancer Progression; January 7-10, 2016; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-c36.
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Torroella-Kouri, Marta, Dayron Rodriguez, Risset Silvera, Mehrjad Nadji, Raul Caso, Gracielena Rodriguez, Ruben R. Gonzalez-Perez, Vijaya Iragavarapu-Charyulu, and Roberto Carrio. "Abstract 398: Tumor microenvironment imposes major alterations and profoundly shapes functional status of macrophages: peritoneal and tumor-associated macrophages from tumor hosts are two very different subpopulations." 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.am2012-398.
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