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      The role IL-1 in tumor-mediated angiogenesis

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          Abstract

          Tumor angiogenesis is one of the hallmarks of tumor progression and is essential for invasiveness and metastasis. Myeloid inflammatory cells, such as immature myeloid precursor cells, also termed myeloid-derived suppressor cells (MDSCs), neutrophils, and monocytes/macrophages, are recruited to the tumor microenvironment by factors released by the malignant cells that are subsequently “educated” in situ to acquire a pro-invasive, pro-angiogenic, and immunosuppressive phenotype. The proximity of myeloid cells to endothelial cells (ECs) lining blood vessels suggests that they play an important role in the angiogenic response, possibly by secreting a network of cytokines/chemokines and inflammatory mediators, as well as via activation of ECs for proliferation and secretion of pro-angiogenic factors. Interleukin-1 (IL-1) is an “alarm,” upstream, pro-inflammatory cytokine that is generated primarily by myeloid cells. IL-1 initiates and propagates inflammation, mainly by inducing a local cytokine network and enhancing inflammatory cell infiltration to affected sites and by augmenting adhesion molecule expression on ECs and leukocytes. Pro-inflammatory mediators were recently shown to play an important role in tumor-mediated angiogenesis and blocking their function may suppress tumor progression. In this review, we summarize the interactions between IL-1 and other pro-angiogenic factors during normal and pathological conditions. In addition, the feasibility of IL-1 neutralization approaches for anti-cancer therapy is discussed.

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          Most cited references 159

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Immunity, inflammation, and cancer.

            Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, malignant conversion, invasion, and metastasis. Inflammation also affects immune surveillance and responses to therapy. Immune cells that infiltrate tumors engage in an extensive and dynamic crosstalk with cancer cells, and some of the molecular events that mediate this dialog have been revealed. This review outlines the principal mechanisms that govern the effects of inflammation and immunity on tumor development and discusses attractive new targets for cancer therapy and prevention. 2010 Elsevier Inc. All rights reserved.
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              Angiogenesis in cancer and other diseases.

               P Carmeliet,  R Jain (2000)
              Pathological angiogenesis is a hallmark of cancer and various ischaemic and inflammatory diseases. Concentrated efforts in this area of research are leading to the discovery of a growing number of pro- and anti-angiogenic molecules, some of which are already in clinical trials. The complex interactions among these molecules and how they affect vascular structure and function in different environments are now beginning to be elucidated. This integrated understanding is leading to the development of a number of exciting and bold approaches to treat cancer and other diseases. But owing to several unanswered questions, caution is needed.
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                28 March 2014
                2014
                : 5
                Affiliations
                The Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences and The Cancer Research Center, Ben-Gurion University of the Negev Beer-Sheva, Israel
                Author notes

                Edited by: Michal Amit Rahat, Technion - Israel Institute for Technology, Israel

                Reviewed by: Jincai Luo, Peking University, China; Luca Vannucci, Academy of Sciences of the Czech Republic, Czech Republic

                *Correspondence: Elena Voronov, The Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences and The Cancer Research Center, Ben-Gurion University of the Negev, Ben Gurion Str., PO Box 653, Beer-Sheva 84105, Israel e-mail: elena@ 123456bgu.ac.il

                This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology.

                †Present address: Yaron Carmi, Department of Pathology, School of Medicine, Stanford University, Palo Alto, USA

                Article
                10.3389/fphys.2014.00114
                3975103
                24734023
                Copyright © 2014 Voronov, Carmi and Apte.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Counts
                Figures: 1, Tables: 0, Equations: 0, References: 159, Pages: 11, Words: 11061
                Categories
                Physiology
                Review Article

                Anatomy & Physiology

                inflammation, il-1α, il-1β, vegf, vegfr1, vegfr2, angiogenesis, myeloid cells

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