Literatura académica sobre el tema "Tumor microenvironment, Extracellular vesicles, Myeloid cells"
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Artículos de revistas sobre el tema "Tumor microenvironment, Extracellular vesicles, Myeloid cells"
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Arkhypov, Ihor, Samantha Lasser, Vera Petrova, et al. "Myeloid Cell Modulation by Tumor-Derived Extracellular Vesicles." International Journal of Molecular Sciences 21, no. 17 (2020): 6319. http://dx.doi.org/10.3390/ijms21176319.
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Extracellular vesicles (EV) can carry proteins, RNA and DNA, thus serving as communication tools between cells. Tumor cells secrete EV, which can be taken up by surrounding cells in the tumor microenvironment as well as by cells in distant organs. Tumor-derived EV (TEV) contain factors induced by tumor-associated hypoxia such as heat shock proteins or a variety of microRNA (miRNA). The interaction of TEV with tumor and host cells can promote cancer angiogenesis, invasion and metastasis. Myeloid cells are widely presented in tissues, comprise the majority of immune cells and play an essential role in immune reactions and tissue remodeling. However, in cancer, the differentiation of myeloid cells and their functions are impaired, resulting in tumor promotion. Such alterations are due to chronic inflammatory conditions associated with cancer and are mediated by the tumor secretome, including TEV. A high capacity of myeloid cells to clear EV from circulation put them in the central position in EV-mediated formation of pre-metastatic niches. The exposure of myeloid cells to TEV could trigger numerous signaling pathways. Progenitors of myeloid cells alter their differentiation upon the contact with TEV, resulting in the generation of myeloid-derived suppressor cells (MDSC), inhibiting anti-tumor function of T and natural killer (NK) cells and promoting thereby tumor progression. Furthermore, TEV can augment MDSC immunosuppressive capacity. Different subsets of mature myeloid cells such as monocytes, macrophages, dendritic cells (DC) and granulocytes take up TEV and acquire a protumorigenic phenotype. However, the delivery of tumor antigens to DC by TEV was shown to enhance their immunostimulatory capacity. The present review will discuss a diverse and complex EV-mediated crosstalk between tumor and myeloid cells in the context of the tumor type, TEV-associated cargo molecules and type of recipient cells.
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Miyazaki, Tsubasa, Eiichi Ishikawa, Narushi Sugii, and Masahide Matsuda. "Therapeutic Strategies for Overcoming Immunotherapy Resistance Mediated by Immunosuppressive Factors of the Glioblastoma Microenvironment." Cancers 12, no. 7 (2020): 1960. http://dx.doi.org/10.3390/cancers12071960.
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Various mechanisms of treatment resistance have been reported for glioblastoma (GBM) and other tumors. Resistance to immunotherapy in GBM patients may be caused by acquisition of immunosuppressive ability by tumor cells and an altered tumor microenvironment. Although novel strategies using an immune-checkpoint inhibitor (ICI), such as anti-programmed cell death-1 antibody, have been clinically proven to be effective in many types of malignant tumors, such strategies may be insufficient to prevent regrowth in recurrent GBM. The main cause of GBM recurrence may be the existence of an immunosuppressive tumor microenvironment involving immunosuppressive cytokines, extracellular vesicles, chemokines produced by glioma and glioma-initiating cells, immunosuppressive cells, etc. Among these, recent research has paid attention to various immunosuppressive cells—including M2-type macrophages and myeloid-derived suppressor cells—that cause immunosuppression in GBM microenvironments. Here, we review the epidemiological features, tumor immune microenvironment, and associations between the expression of immune checkpoint molecules and the prognosis of GBM. We also reviewed various ongoing or future immunotherapies for GBM. Various strategies, such as a combination of ICI therapies, might overcome these immunosuppressive mechanisms in the GBM microenvironment.
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Fernández-Delgado, Irene, Diego Calzada-Fraile, and Francisco Sánchez-Madrid. "Immune Regulation by Dendritic Cell Extracellular Vesicles in Cancer Immunotherapy and Vaccines." Cancers 12, no. 12 (2020): 3558. http://dx.doi.org/10.3390/cancers12123558.
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Extracellular vesicles (EVs) play a crucial role in intercellular communication as vehicles for the transport of membrane and cytosolic proteins, lipids, and nucleic acids including different RNAs. Dendritic cells (DCs)-derived EVs (DEVs), albeit variably, express major histocompatibility complex (MHC)-peptide complexes and co-stimulatory molecules on their surface that enable the interaction with other immune cells such as CD8+ T cells, and other ligands that stimulate natural killer (NK) cells, thereby instructing tumor rejection, and counteracting immune-suppressive tumor microenvironment. Malignant cells oppose this effect by secreting EVs bearing a variety of molecules that block DCs function. For instance, tumor-derived EVs (TDEVs) can impair myeloid cell differentiation resulting in myeloid-derived suppressor cells (MDSCs) generation. Hence, the unique composition of EVs makes them suitable candidates for the development of new cancer treatment approaches including prophylactic vaccine targeting oncogenic pathogens, cancer vaccines, and cancer immunotherapeutics. We offer a perspective from both cell sides, DCs, and tumor cells, on how EVs regulate the antitumor immune response, and how this translates into promising therapeutic options by reviewing the latest advancement in DEV-based cancer therapeutics.
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Colombo, Michela, Domenica Giannandrea, Elena Lesma, Andrea Basile, and Raffaella Chiaramonte. "Extracellular Vesicles Enhance Multiple Myeloma Metastatic Dissemination." International Journal of Molecular Sciences 20, no. 13 (2019): 3236. http://dx.doi.org/10.3390/ijms20133236.
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Extracellular vesicles (EVs) represent a heterogeneous group of membranous structures shed by all kinds of cell types, which are released into the surrounding microenvironment or spread to distant sites through the circulation. Therefore, EVs are key mediators of the communication between tumor cells and the surrounding microenvironment or the distant premetastatic niche due to their ability to transport lipids, transcription factors, mRNAs, non-coding regulatory RNAs, and proteins. Multiple myeloma (MM) is a hematological neoplasm that mostly relies on the bone marrow (BM). The BM represents a highly supportive niche for myeloma establishment and diffusion during the formation of distant bone lesions typical of this disease. This review represents a survey of the most recent evidence published on the role played by EVs in supporting MM cells during the multiple steps of metastasis, including travel and uptake at distant premetastatic niches, MM cell engraftment as micrometastasis, and expansion to macrometastasis thanks to EV-induced angiogenesis, release of angiocrine factors, activation of osteolytic activity, and mesenchymal cell support. Finally, we illustrate the first evidence concerning the dual effect of MM-EVs in promoting both anti-tumor immunity and MM immune escape, and the possible modulation operated by pharmacological treatments.
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Saltarella, Ilaria, Aurelia Lamanuzzi, Benedetta Apollonio, et al. "Role of Extracellular Vesicle-Based Cell-to-Cell Communication in Multiple Myeloma Progression." Cells 10, no. 11 (2021): 3185. http://dx.doi.org/10.3390/cells10113185.
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Multiple myeloma (MM) progression closely depends on the bidirectional crosstalk between tumor cells and the surrounding microenvironment, which leads to the creation of a tumor supportive niche. Extracellular vesicles (EVs) have emerged as key players in the pathological interplay between the malignant clone and near/distal bone marrow (BM) cells through their biologically active cargo. Here, we describe the role of EVs derived from MM and BM cells in reprogramming the tumor microenvironment and in fostering bone disease, angiogenesis, immunosuppression, drug resistance, and, ultimately, tumor progression. We also examine the emerging role of EVs as new therapeutic agents for the treatment of MM, and their potential use as clinical biomarkers for early diagnosis, disease classification, and therapy monitoring.
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Watanabe, Takashi. "Realization of Osteolysis, Angiogenesis, Immunosuppression, and Drug Resistance by Extracellular Vesicles: Roles of RNAs and Proteins in Their Cargoes and of Ectonucleotidases of the Immunosuppressive Adenosinergic Noncanonical Pathway in the Bone Marrow Niche of Multiple Myeloma." Cancers 13, no. 12 (2021): 2969. http://dx.doi.org/10.3390/cancers13122969.
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Angiogenesis and immunosuppression promote multiple myeloma (MM) development, and osteolysis is a primary feature of MM. Although immunomodulatory drugs and proteasome inhibitors (PIs) markedly improve the survival of patients with MM, this disease remains incurable. In the bone marrow niche, a chain of ectoenzymes, including CD38, produce immunosuppressive adenosine, inhibiting T cell proliferation as well as immunosuppressive cells. Therefore, anti-CD38 antibodies targeting myeloma cells have the potential to restore T cell responses to myeloma cells. Meanwhile extracellular vesicles (EVs) containing microRNAs, proteins such as cytokines and chemokines, long noncoding RNAs, and PIWI-interacting RNAs have been shown to act as communication tools in myeloma cell/microenvironment interactions. Via EVs, mesenchymal stem cells allow myeloma cell dissemination and confer PI resistance, whereas myeloma cells promote angiogenesis, myeloid-derived suppressor cell proliferation, and osteoclast differentiation and inhibit osteoblast differentiation. In this review, to understand key processes of MM development involving communication between myeloma cells and other cells in the tumor microenvironment, EV cargo and the non-canonical adenosinergic pathway are introduced, and ectoenzymes and EVs are discussed as potential druggable targets for the treatment of MM patients.
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Awadasseid, Annoor, Yanling Wu, and Wen Zhang. "Extracellular Vesicles (Exosomes) as Immunosuppressive Mediating Variables in Tumor and Chronic Inflammatory Microenvironments." Cells 10, no. 10 (2021): 2533. http://dx.doi.org/10.3390/cells10102533.
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Exosomes are extracellular vesicles released by most of the eukaryotic cells. Exosomes’ components include proteins, lipids, microRNA, circular RNA, long noncoding RNA, DNA, etc. Exosomes may carry both pro and anti-inflammatory cargos; however, exosomes are predominantly filled with immunosuppressive cargos such as enzymes and microRNAs in chronic inflammation. Exosomes have surfaced as essential participants in physiological and pathological intercellular communication. Exosomes may prevent or promote the formation of an aggressive tumor and chronic inflammatory microenvironments, thus influencing tumor and chronic inflammatory progression as well as clinical prognosis. Exosomes, which transmit many signals that may either enhance or constrain immunosuppression of lymphoid and myeloid cell populations in tumors, are increasingly becoming recognized as significant mediators of immune regulation in cancer. In this review, we outline the function of exosomes as mediators of immunosuppression in tumor and chronic inflammatory microenvironments, with the aim to improve cancer therapy.
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Hoelzinger, Dominique B., Sophia J. Quinton, Denise K. Walters, Renee C. Tschumper, and Diane F. Jelinek. "Proteomic and Biological Analysis of Myeloma Cell Derived Extracellular Vesicles." Blood 132, Supplement 1 (2018): 5605. http://dx.doi.org/10.1182/blood-2018-99-116926.
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Abstract Intercellular communication between multiple myeloma (MM) cells and the normal bone marrow stroma leads to a modification of the bone marrow microenvironment, which favors tumor progression. New developments in extracellular vesicle (EV) research suggest that this diverse population of vesicles, released by cancer cells including MM cells, express transmembrane proteins and carry cargo that can modify recipient cells in myriad ways. In particular, tumor-derived EVs have been shown to create permissive microenvironments that lead to metastatic colonization by circulating tumor cells. As we have previously shown that MM EVs can enhance proliferation of recipient MM cells, we hypothesize that MM EVs can potentially play a much larger role in MM development and progression. In order to understand the scope of potential EV roles in MM, we executed a comprehensive proteomic analysis of the cargo of MM EVs. We isolated EVs from patient derived MM cell lines that represent the most common genetic variants of this tumor, and used in vitro generated plasma cells (IVPCs) as a reference population. In a first pass analysis, we selected proteins that were expressed ≥3 fold higher in MM EVs than in IVPC EVs, and this analysis identified 306 proteins. Of interest, included in the 306 differentially proteins were several involved in the regulation of cell adhesion such as members of the a disintegrin and metalloprotease domain (ADAM8, 9, 10, 13, 15 and 22) family, which are also associated with inhibition of cell proliferation. Moreover, CEACAM1, PTPRK, and CDH2, which are also linked to cellular adhesion, were also expressed at a higher level in MM EVs. Various proteins linked to myeloma cell biology were likewise found to be over-represented in MM EVs, and these include BCMA, ITGAV, ITGB5, IL6ST (gp130), CD276 (B7-H3), and CD28. As we are most interested in biologically relevant and actionable proteins present uniquely in MM derived EVs, we filtered from our data proteins that were also present in EVs from IVPCs. We further filtered out proteins known to be present in EVs from normal cells. This filtering strategy reduced the number of interesting candidates to 8, which included CD28, MET, TRKC, and ADAM15. Thus far, we have confirmed the presence of these 4 proteins in a panel of MM EVs, and we are currently in the process of validating additional candidate cargo proteins for their biological role in enhancing tumor cell proliferation and/or protection from apoptosis. In summary, EV proteomic analysis of cell lines representing MM genetic subtypes can lead to the identification of biologically relevant proteins transported systemically by EVs as well as suggest novel biomarkers that are easily detectable in plasma and may permit earlier recognition of disease progression in patients with MM. Disclosures No relevant conflicts of interest to declare.
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Cariello, Mariaconcetta, Angela Squilla, Martina Piacente, Giorgia Venutolo, and Alessio Fasano. "Drug Resistance: The Role of Exosomal miRNA in the Microenvironment of Hematopoietic Tumors." Molecules 28, no. 1 (2022): 116. http://dx.doi.org/10.3390/molecules28010116.
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Extracellular vesicles (EVs), including exosomes, have an important role thanks to their ability to communicate and exchange information between tumor cells and the tumor microenvironment (TME), and have also been associated with communicating anti-cancer drug resistance (DR). The increase in proliferation of cancer cells alters oxygen levels, which causes hypoxia and results in a release of exosomes by the cancer cells. In this review, the results of studies examining the role of exosomal miRNA in DR, and their mechanism, are discussed in detail in hematological tumors: leukemia, lymphoma, and multiple myeloma. In conclusion, we underline the exosome’s function as a possible drug delivery vehicle by understanding its cargo. Engineered exosomes can be used to be more specific for personalized therapy.
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Matthaios, Dimitrios, Maria Tolia, Davide Mauri, Konstantinos Kamposioras, and Michalis Karamouzis. "YAP/Hippo Pathway and Cancer Immunity: It Takes Two to Tango." Biomedicines 9, no. 12 (2021): 1949. http://dx.doi.org/10.3390/biomedicines9121949.
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Hippo pathway with its main molecule YAP is a crucial pathway for development, tissue homeostasis, wound healing, tissue regeneration, and cancer. In this review, we discuss the multiple effects of the YAP/Hippo pathway in the immune system and cancer. We analyzed a series of effects: extracellular vesicles enhanced immunity through inhibition of LATS1/2, ways of modulation of the tumor microenvironment, YAP- and TAZ-mediated upregulation of PDL1, high expression of YAP and PDL1 in EGFR-TKI-resistant cells, enhanced YAP activity in inflammation, and the effect of the Hippo pathway on T cells, B cells, Tregs, macrophages, and myeloid-derived suppressor cells (MDSCs). These pleiotropic effects render the YAP and Hippo pathway a key pathway for exploitation in the future, in order to enhance our immunotherapy treatment strategies in oncology.
Tesis sobre el tema "Tumor microenvironment, Extracellular vesicles, Myeloid cells"
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Sartori, Sara. "Tumor-derived exosomes favor immunosuppression and metastatic spread by acting on myeloid cells." Doctoral thesis, 2019. http://hdl.handle.net/11562/994963.
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It is widely recognized that the immune system can be highly affected by tumors through a plethora of mechanisms that allow avoiding an efficient recognition and eradication of cancer cells. Among these mechanisms, tumor secretome, including tumor-derived soluble factors (TDSFs) and, more recently, extracellular vesicles (EVs), is currently drawing much attention in the immune-oncology field. Particularly, by interacting either with stromal or other tumor cells, tumor-derived exosomes (TEX) have been demonstrated as key regulators in cancer development, as well as on the metastatic process. Since myeloid-derived suppressor cells (MDSCs) are critical contributors to the aforementioned processes, we investigated the TEX-MDSCs interaction, highlighting the main functional consequences of this crosstalk. Indeed, we could demonstrate a TEX-mediated effect on MDSC suppressive functions, which was even more striking in the case of bone-marrow naïve monocytes. Furthermore, we demonstrated that this is mainly mediated by iNOS engagement on myeloid cells, possibly induced by molecules enriched within TEX. In addition, the injection of TEX derived from high metastatic cancer cells in naïve tumor-free mice before the tumor challenge with a low metastatic cell line induced an increased spread of cancer cells in the lungs of TEX-treated mice. In the attempt to dampen TEX detrimental effects in tumor models, we blocked exosome secretion through GW4869 drug administration, which did not ameliorate the spread of metastatic cells. On the contrary, by targeting one of the TEX-downstream mediators, i.e. a member of the S100 proteins family, tumor-bearing mice displayed a restrained suppressive tumor network and a strong reduction in the metastatic incidence. Finally, we demonstrated that S100A8/A9 sera levels negatively correlated with distant metastasis-free survival in pancreatic ductal adenocarcinoma (PDAC) patients. In conclusion, our preliminary data highlighted the urgency of developing novel and more effective therapeutic approaches based on a full characterization of TEX-induced pathways in myeloid cells within the local tumor milieu and, moreover, at distal sites of metastasis.
Capítulos de libros sobre el tema "Tumor microenvironment, Extracellular vesicles, Myeloid cells"
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S. Chauhan, Deepak, Priyanka Mudaliar, Soumya Basu, Jyotirmoi Aich, and Manash K. Paul. "Tumor-Derived Exosome and Immune Modulation." In Extracellular Vesicles - Role in Diseases Pathogenesis and Therapy [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103718.
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Tumor cells, like most other cells, release exosomes called tumor-derived exosomes (TEX) and are vital for intercellular communication. TEX are membrane-bound extracellular vesicles (EVs), containing unique cargo reminiscent of the parent tumor cells and possess immunomodulatory functions. TEX carries factors that directly promote immunosuppression in the tumor microenvironment and indirectly attract immunosuppressive T-regulatory (Treg) cells. The tumor-secreted exosomes can transfer their cargo by multiple mechanisms like fusion, phagocytosis, and receptor-mediated endocytosis, activating the recipient cells. TEX directly engages and releases cytokines, inactivating natural killer (NK) cells and T-cells and activating apoptosis. Tumor-derived exosomes also release soluble factors to suppress dendritic cell (DC) maturation while activating the expansion of immune-suppressive cells like Myeloid-derived suppressor cells (MDSCs) and Regulatory T (Treg) cells. Several studies have shown the relevance of TEX containing tumor-associated antigens (TAA) in reducing the efficacy of cancer immunotherapy and adoptive cell therapy. Hence understanding the basic biology and mechanism of TEX-mediated immunosuppression is critical in discovering cancer biomarkers and finding better immunotherapy and cell therapy approaches. In this chapter, we have discussed TEX biogenesis, TEX\'s structural and molecular features, TEX-mediated immunosuppression, and its relation to immunotherapy.
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Helmy Thabet, Eman. "Roles of Extracellular Vesicles in Cancer Metastasis." In Extracellular Vesicles - Role in Diseases Pathogenesis and Therapy [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103798.
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Extracellular vesicles (EVs) are biological active vesicles and carriers of information in intercellular communication. In cancer settings, EVs especially exosomes (Exo), play a focal role in modulating the tumor microenvironment mainly by increasing tumor proliferation, facilitating the crosstalk between tumor and tumor-neighboring cells, and influencing the host immune response. Amongst these functions in tumor growth, Exo modulate fundamental steps of tumor progression, such as growth, invasion, and immune modulation. On the endocrine level, Exo released from tumors were shown to mediate distant cell-cell communication processes via secretory factors and miRNAs, which result in the set-up of pro-tumorigenic microenvironments supportive of metastatic dissemination. This is achieved through processes such as fibroblast activation, extracellular matrix ECM production, angiogenesis, and immune modulation.
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Basu, Bhaskar, and Subhajit Karmakar. "The Role of Extracellular Vesicles in the Progression of Tumors towards Metastasis." In Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101635.
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Extracellular vesicles (EVs) are cell-derived lipid membrane bound vesicles that serve as mediators of intercellular communication. EVs have been found to regulate a wide range of cellular processes through the transference of genetic, protein and lipid messages from the host cell to the recipient cell. Unsurprisingly, this major mode of intracellular communication would be abrogated in cancer. Ever increasing evidence points towards a key role of EVs in promoting tumor development and in contributing to the various stages of metastasis. Tumor released EVs have been shown to facilitate the transference of oncogenic proteins and nucleic acids to other tumor cells and to the surrounding stromal cells, thereby setting up a tumor permissive microenvironment. EVs released from tumor cells have been shown to promote extracellular matrix (ECM) remodeling through the modulation of neighboring tumor cells and stromal cells. EVs released from disseminated tumor cells have been reported to attract circulating tumor cells (CTCs) via chemotaxis and induce the production of specific extracellular matrix components from neighboring stromal cells so as to support the growth of metastatic cells at the secondary tumor site. Circulating levels of tumor derived EVs of patients have been correlated with incidence of metastasis and disease relapse.
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Yadav, Joni, Nikita Aggarwal, Apoorva Chaudhary, et al. "Role of Exosomes in Tumor Induced Neo-Angiogenesis." In Tumor Angiogenesis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104400.
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Exosomes are the nanovesicles, belonging to the type of extracellular vesicles (EVs), produced by normal as well as tumor cells and function as a mode in cell-to-cell communication. Tumor cells utilize various approach to communicate with neighboring cells for facilitating tumor invasion and progression, one of these approaches has been shown through the release of exosomes. Tumor-derived exosomes (TEX) have the ability to reprogram/modulate the activity of target cells due to their genetic and molecular cargo. Such exosomes target endothelial cells (among others) in the tumor microenvironment (TME) to promote angiogenesis which is an important element for solid tumor growth and metastasis. So, exosomes play a vital role in cancer invasiveness and progression by harboring various cargoes that could accelerate angiogenesis. Here first, we will present an overview of exosomes, their biology, and their role in different cancer models. Then, we will emphasis on exosomes derived from tumor cells as tumor angiogenesis mediators with a particular importance on the underlying mechanisms in various cancer origins. In the end, we will unveil the therapeutic potential of tumor derived exosomes as drug delivery vehicles against angiogenesis.
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Yadav, Joni, Nikita Aggarwal, Apoorva Chaudhary, et al. "Role of Exosomes in Tumor Induced Neo-Angiogenesis." In Tumor Angiogenesis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104400.
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Exosomes are the nanovesicles, belonging to the type of extracellular vesicles (EVs), produced by normal as well as tumor cells and function as a mode in cell-to-cell communication. Tumor cells utilize various approach to communicate with neighboring cells for facilitating tumor invasion and progression, one of these approaches has been shown through the release of exosomes. Tumor-derived exosomes (TEX) have the ability to reprogram/modulate the activity of target cells due to their genetic and molecular cargo. Such exosomes target endothelial cells (among others) in the tumor microenvironment (TME) to promote angiogenesis which is an important element for solid tumor growth and metastasis. So, exosomes play a vital role in cancer invasiveness and progression by harboring various cargoes that could accelerate angiogenesis. Here first, we will present an overview of exosomes, their biology, and their role in different cancer models. Then, we will emphasis on exosomes derived from tumor cells as tumor angiogenesis mediators with a particular importance on the underlying mechanisms in various cancer origins. In the end, we will unveil the therapeutic potential of tumor derived exosomes as drug delivery vehicles against angiogenesis.
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Jain, Sapna, and Manjari Singh. "Engineering of Extracellular Vesicles as Nano Therapy for Breast Cancer." In Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101149.
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Extracellular vesicles are membrane-derived nanoparticles that represent a novel mechanism of cell-to-cell communication. It is well reported that EVs play a central role in the tumor microenvironment by mediating intercellular signaling among cancer cells. This has resulted in the development of therapeutic strategies targeting various EV signaling pathways in cancer. However, because of their small size and endogenous origin, they have been extensively explored for cancer drug delivery. Hence, owing to their natural ability to mediate intercellular communication, high stability, and low immunogenicity, they have emerged as an attractive platform for cancer treatment. However, limited production and insufficient loading with therapeutic moieties are some of the issues constraining their clinical translation. In this chapter, recent research studies performed in an attempt to develop EVs as cancer biomarkers or drug delivery systems will be discussed. Further, it will also discuss various strategies such as direct and indirect cell surface modification, which can be employed to make EVs successful as cancer therapeutics. Furthermore, it will highlight the current and completed clinical trials using naturally derived EVs as cancer therapeutics.
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Nakaoka, Ai, Kana Kobayashi, Mennaallah Hassan, and Ryohei Sasaki. "Exosomes in Cancer Diagnosis and Radiation Therapy." In Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101684.
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Exosomes are a subgroup of extracellular vesicles that are released by all types of cells, including tumor cells, and mediate intercellular communication via the transport of various intracellular components, including microRNAs, messenger RNAs, and proteins. Radiation produces reactive oxygen species and induces DNA double-strand break in cancer cells and normal cells. Cancer cells have severe damage and die by irradiation, but normal cells can keep proliferation with their high DNA repair ability. Irradiated cells generate communication signals and cause biological changes in neighboring or distant non-irradiated cells. This review outlines the role of exosomes in radiation therapy. In the tumor microenvironment, exosomes are considered to regulate cell survival, migration, and resistance to therapy by interacting with vascular endothelial cells and various types of immune cells. Nowadays, radiation therapy is typically combined with immunotherapy. Regulation of the activity of exosomes may overcome the problem of resistance to immunotherapy. Furthermore, exosomes can attenuate resistance to chemotherapy by transporting certain types of microRNA. The current evidence suggests that exosomes may be useful in the diagnosis and treatment of cancer in the future.
Actas de conferencias sobre el tema "Tumor microenvironment, Extracellular vesicles, Myeloid cells"
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Kim, Jayoung, Samantha Morley, Minh Le, et al. "Abstract 1658: Enhanced shedding of extracellular vesicles from amoeboid prostate cancer cells: Potential effects on the tumor microenvironment." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1658.
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