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      Role of Chemokines in Non-Small Cell Lung Cancer: Angiogenesis and Inflammation

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          Abstract

          Non-small cell lung cancer (NSCLC) is one of the most common types of aggressive cancer. The tumor tissue, which shows an active angiogenesis, is composed of neoplastic and stromal cells, and an abundant inflammatory infiltrate. Angiogenesis is important to support tumor growth, while infiltrating cells contribute to the tumor microenvironment through the secretion of growth factors, cytokines and chemokines, important molecules in the progression of the disease. Chemokines are important in development, activation of the immune response, and physiological angiogenesis. Chemokines have emerged as important regulators in the pathophysiology of cancer. These molecules are involved in the angiogenesis/angiostasis balance and in the recruitment of tumor infiltrating hematopoietic cells. In addition, chemokines promote tumor cell survival, as well as the directing and establishment of tumor cells to metastasis sites. The findings summarized here emphasize the central role of chemokines as modulators of tumor angiogenesis and their potential role as therapeutic targets in the inflammatory process of NSCLC angiogenesis.

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          Most cited references 154

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          Chemokines: a new classification system and their role in immunity.

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            Endothelial cell migration during angiogenesis.

            Endothelial cell migration is essential to angiogenesis. This motile process is directionally regulated by chemotactic, haptotactic, and mechanotactic stimuli and further involves degradation of the extracellular matrix to enable progression of the migrating cells. It requires the activation of several signaling pathways that converge on cytoskeletal remodeling. Then, it follows a series of events in which the endothelial cells extend, contract, and throw their rear toward the front and progress forward. The aim of this review is to give an integrative view of the signaling mechanisms that govern endothelial cell migration in the context of angiogenesis.
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              CD8+ T cells infiltrated within cancer cell nests as a prognostic factor in human colorectal cancer.

              The pathophysiological significance of tumor infiltrating lymphocytes remains controversial. To clarify their role, we performed clinicopathological analysis of CD8+ T cells in 131 cases of human colorectal cancer. CD8+ T cells were classified into three groups by their localization: (a) those infiltrated within cancer cell nests; (b) those distributed in the cancer stroma; and (c) those present along the invasive margin (tumor-host interface). Of these, CD8+ T cells within cancer cell nests were most significantly associated with a better survival of patients by both mono- and multivariate analyses. The impact on survival was similar to that of Dukes' staging. Granzyme B+ cytoplasmic granules were detected in lymphocytes within cancer cell nests, confirming their activated, cytotoxic phenotype. CD8 and Ki-67 double immunohistochemistry confirmed higher proliferative activity of CD8+ T cells within cancer cell nests. Our data suggested that human colorectal cancer tissue was infiltrated by various numbers of T cells that had cytotoxic phenotype, contributing to a better survival of patients. This infiltration of colorectal cancer cell nests by CD8+ T cells could be a novel prognostic factor.
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                Author and article information

                Journal
                J Cancer
                J Cancer
                jca
                Journal of Cancer
                Ivyspring International Publisher (Sydney )
                1837-9664
                2015
                7 August 2015
                : 6
                : 10
                : 938-952
                Affiliations
                1. Department of Biochemistry Research, National Institute of Respiratory Diseases “Ismael Cosío Villegas”, Mexico City, Mexico.
                2. Laboratory of Research on Rheumatic Diseases, National Institute of Respiratory Diseases “Ismael Cosío Villegas”, Mexico City, Mexico.
                3. Department of Comparative Biology, Faculty of Sciences, National Autonomous University of Mexico, Mexico City, Mexico.
                4. Laboratory of Research on Genomics, Genetics and Bioinformatics. Tower of Haemato-oncology, Children´s Hospital of Mexico “Federico Gomez”, Mexico City, Mexico.
                Author notes
                ✉ Corresponding author: Department of Biochemistry Research, National Institute of Respiratory Diseases “Ismael Cosío Villegas”, Mexico City, Mexico. Calzada de Tlalpan 4502, Tlalpan, Ciudad de México, D.F. 14080, México. Phone +52 (55) 5487 1705; E-mail: selma.rivas@ 123456iner.gob.mx .

                Competing Interests: No competing interests were disclosed.

                Article
                jcav06p0938
                10.7150/jca.12286
                4543754
                © 2015 Ivyspring International Publisher. Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. See http://ivyspring.com/terms for terms and conditions.
                Categories
                Review

                Oncology & Radiotherapy

                chemokines, cytokines, angiogenesis, inflammation, non-small cell lung cancer.

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