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1. Full Text Therapeutic efficacy and immunological response of CCL5 antagonists in models of contact skin reaction
by Canavese, Miriam and Altruda, Fiorella and Silengo, Lorenzo
PLoS ONE, ISSN 1932-6203, 01/2010, Volume 5, Issue 1, p. e8725
Skin-infiltrating T-cells play a predominant role in allergic and inflammatory skin diseases such as atopic dermatitis, psoriasis and allergic contact... 
CHEMOKINE SYSTEM | DERMATITIS | MULTIDISCIPLINARY SCIENCES | DISEASE | KERATINOCYTES | INTERFERENCE | RECEPTORS | MET-RANTES | PSORIASIS | Immunohistochemistry | Dermatitis, Contact - immunology | Animals | Dermatitis, Contact - drug therapy | Cells, Cultured | Oxazolone - toxicity | Female | Mice | Chemokine CCL5 - antagonists & inhibitors | Disease Models, Animal | Psoriasis | Atopic dermatitis | Analysis | Skin | Inflammation | T cells | Health aspects | Chemotactic factors | CC chemokine receptors | Multiple sclerosis | Disease | Leukocyte migration | Laboratories | Pathogenesis | RANTES | Nervous system | Antagonists | Lymphocytes T | Biology | Biochemistry | Haptens | Dermatitis | Mimicry | CCR1 protein | Keratin | Cell activation | Immunology | Rodents | Skin diseases | Trends | Ultrasonic testing | CCR5 protein | Immune response | Cytokines | Hypersensitivity | Neutrophils | Keratinocytes | Allergies | Contact dermatitis | Ligands | Cell migration | Chemokines
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2. Full Text Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133+ Ovarian Cancer Stem‐Like Cells via NF‐κB‐Mediated MMP‐9 Upregulation
by Long, Haixia and Xie, Rongkai and Xiang, Tong and Zhao, Zhongquan and Lin, Sheng and Liang, Zhiqing and Chen, Zhengtang and Zhu, Bo
STEM CELLS, ISSN 1066-5099, 10/2012, Volume 30, Issue 10, pp. 2309 - 2319
The concept of cancer stem cells (CSCs) proposes that solely CSCs are capable of generating tumor metastases. However, how CSCs maintain their invasion and... 
Ovarian | Cancer stem cells | CCL5 | Migration | Invasion | Humans | Gene Expression Regulation, Neoplastic | Glycoproteins - metabolism | Ovarian Neoplasms - pathology | Peptides - genetics | Receptors, CCR5 - genetics | NF-kappa B - metabolism | Antigens, CD - genetics | Biomarkers, Tumor | Chemokine CCL5 - antagonists & inhibitors | Antigens, CD - metabolism | Ovarian Neoplasms - genetics | Receptors, CCR5 - metabolism | Peptides - metabolism | Matrix Metalloproteinase 9 - genetics | Receptors, CCR3 - genetics | Female | Matrix Metalloproteinase 9 - secretion | Ovarian Neoplasms - metabolism | Neoplastic Stem Cells - physiology | Ovary - metabolism | Receptors, CCR3 - antagonists & inhibitors | Glycoproteins - genetics | Ovary - pathology | Signal Transduction | AC133 Antigen | Receptors, CCR1 - genetics | NF-kappa B - genetics | Chemokine CCL5 - genetics | Cell Line, Tumor | Primary Cell Culture | Neoplasm Invasiveness - genetics | Cell Movement | Receptors, CCR1 - antagonists & inhibitors
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3. Full Text CC chemokine CCL5 plays a central role impacting infarct size and post-infarction heart failure in mice
by Montecucco, Fabrizio and Braunersreuther, Vincent and Lenglet, Sébastien and Delattre, Benedicte M.A and Pelli, Graziano and Buatois, Vanessa and Guilhot, Florence and Galan, Katia and Vuilleumier, Nicolas and Ferlin, Walter and Fischer, Nicolas and Vallée, Jean-Paul and Kosco-Vilbois, Marie and MacH, François
European Heart Journal, ISSN 0195-668X, 08/2012, Volume 33, Issue 15, pp. 1964 - 1974
The chemokine CCL5 plays a critical role as neutrophil and macrophage activator do in atherosclerosis and myocardial infarction. Thus, we investigated whether... 
Heart failure | Myocardial infarction | Leucocytes | CARDIAC & CARDIOVASCULAR SYSTEMS | INHIBITION | INFLAMMATION | CLINICAL-IMPLICATIONS | INJURY | DYSFUNCTION | ISCHEMIA-REPERFUSION | NEUTROPHIL RECRUITMENT | ACUTE-MYOCARDIAL-INFARCTION | Macrophages - physiology | Myocardial Ischemia - metabolism | Antibodies, Monoclonal - pharmacology | Mice, Inbred C57BL | Neutrophils - physiology | Organ Size - physiology | Survival Rate | Heart Failure - pathology | Chemokine CCL5 - physiology | Chemokine CCL5 - antagonists & inhibitors | Myocardial Reperfusion - methods | Chemotaxis, Leukocyte - physiology | Neutrophil Infiltration - physiology | Collagen - metabolism | Matrix Metalloproteinase 9 - metabolism | Animals | Ligation | Matrix Metalloproteinase 8 - metabolism | Myocardial Infarction - pathology | Mice | Body Weight - physiology | Monocytes - physiology | Chronic Disease | Chemokine CCL5 - immunology
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4. Full Text CCL5/CCR5 axis induces vascular endothelial growth factor-mediated tumor angiogenesis in human osteosarcoma microenvironment
by Wang, Shih-Wei and Wang, Shih-Wei and Liu, Shih-Chia and Sun, Hui-Lung and Huang, Te-Yang and Chan, Chia-Han and Yang, Chen-Yu and Yeh, Hung-I and Huang, Yuan-Li and Chou, Wen-Yi and Lin, Yu-Min and Tang, Chih-Hsin
Carcinogenesis, ISSN 0143-3334, 01/2015, Volume 36, Issue 1, pp. 104 - 114
This study reveals that CCL5/CCR5 axis promotes VEGF expression in human osteosarcoma cells, and contributes to tumor angiogenesis through PKC... 
PROGENITOR CELLS | HYPOXIA-INDUCIBLE FACTOR | PROTEIN-KINASE-C | ACTIVATION | ONCOLOGY | SIGNALING PATHWAY | RANTES | BREAST-CANCER METASTASIS | PROSTATE-CANCER | EXPRESSION | RECEPTOR TRANSACTIVATION | RNA, Small Interfering - genetics | Cell Proliferation | Tissue Array Analysis | Humans | Receptors, CCR5 - genetics | Tumor Microenvironment | Culture Media, Conditioned - pharmacology | Male | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Bone Neoplasms - pathology | Chemokine CCL5 - antagonists & inhibitors | Chorioallantoic Membrane - pathology | Immunoenzyme Techniques | Bone Neoplasms - metabolism | Receptors, CCR5 - metabolism | Flow Cytometry | Chromatin Immunoprecipitation | Bone Neoplasms - blood supply | Osteosarcoma - blood supply | Chemokine CCL5 - metabolism | Tumor Cells, Cultured | Real-Time Polymerase Chain Reaction | Osteosarcoma - metabolism | RNA, Messenger - genetics | Chorioallantoic Membrane - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Chick Embryo | Blotting, Western | Xenograft Model Antitumor Assays | Animals | Mice, Nude | Chemokine CCL5 - genetics | Receptors, CCR5 - chemistry | Mice | Neovascularization, Pathologic - metabolism | Osteosarcoma - pathology | Cell Movement
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5. Full Text Tumoral Immune Cell Exploitation in Colorectal Cancer Metastases Can Be Targeted Effectively by Anti-CCR5 Therapy in Cancer Patients
by Halama, Niels and Zoernig, Inka and Berthel, Anna and Kahlert, Christoph and Klupp, Fee and Suarez-Carmona, Meggy and Suetterlin, Thomas and Brand, Karsten and Krauss, Juergen and Lasitschka, Felix and Lerchl, Tina and Luckner-Minden, Claudia and Ulrich, Alexis and Koch, Moritz and Weitz, Juergen and Schneider, Martin and Buechler, Markus W and Zitvogel, Laurence and Herrmann, Thomas and Benner, Axel and Kunz, Christina and Luecke, Stephan and Springfeld, Christoph and Grabe, Niels and Falk, Christine S and Jaeger, Dirk
Cancer Cell, ISSN 1535-6108, 04/2016, Volume 29, Issue 4, pp. 587 - 601
The immune response influences the clinical course of colorectal cancer (CRC). Analyzing the invasive margin of human CRC liver metastases, we identified a... 
BREAST-CANCER | HEPATOCELLULAR-CARCINOMA | ANTAGONIST | ONCOLOGY | MIGRATION INHIBITORY FACTOR | IMMUNOTHERAPY | INFLAMMATION | EXPRESSION | CHEMOKINE RECEPTOR CCR5 | CHEMOTHERAPY | PROGRESSION | CELL BIOLOGY | Liver Neoplasms - secretion | Lung Neoplasms - drug therapy | Clodronic Acid - pharmacology | Apoptosis - drug effects | Cyclohexanes - pharmacology | Humans | Neoplasm Proteins - physiology | Neoplasm Proteins - antagonists & inhibitors | Molecular Targeted Therapy | Chemokine CCL5 - secretion | Chemokine CCL5 - antagonists & inhibitors | Cyclohexanes - therapeutic use | Macrophages - secretion | Receptors, CCR5 - metabolism | STAT3 Transcription Factor - physiology | Lung Neoplasms - secondary | Tumor Cells, Cultured | Liver Neoplasms - secondary | Pyridines - therapeutic use | Triazoles - therapeutic use | NG-Nitroarginine Methyl Ester - pharmacology | Tumor Microenvironment - drug effects | Neoplasm Invasiveness | Adenocarcinoma - immunology | Liver Neoplasms - drug therapy | Chemokines - physiology | Phenylurea Compounds - therapeutic use | Receptors, CCR5 - drug effects | Liver Neoplasms - immunology | Adenocarcinoma - drug therapy | Chemotaxis | Adenocarcinoma - secondary | Triazoles - pharmacology | Pilot Projects | Chemokine CCL5 - biosynthesis | Colorectal Neoplasms - immunology | Interferon-alpha - secretion | Survival Analysis | Macrophages - drug effects | Lymphocytes, Tumor-Infiltrating - secretion | Clinical Trials, Phase I as Topic | Lymphocytes, Tumor-Infiltrating - immunology | Care and treatment | Liver | Colorectal cancer | Metastasis | T cells | Health aspects | Cancer | Macrophages
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6. Full Text CCL5 neutralization restricts cancer growth and potentiates the targeting of PDGFRβ in colorectal carcinoma
by Cambien, Béatrice and Richard-Fiardo, Peggy and Karimdjee, Babou F and Martini, Violette and Ferrua, Bernard and Pitard, Bruno and Schmid-Antomarchi, Heidy and Schmid-Alliana, Annie
PLoS ONE, ISSN 1932-6203, 11/2011, Volume 6, Issue 12, p. e28842
Increased CCL5 levels are markers of an unfavourable outcome in patients with melanoma, breast, cervical, prostate, gastric or pancreatic cancer. Here, we have... 
CCR5 ANTAGONIST | CELLS | GASTRIC-CANCER | RANTES LEVELS | MULTIDISCIPLINARY SCIENCES | TYROSINE KINASES | COLON | TUMOR STROMA | FACTOR RECEPTOR | EXPRESSION | BREAST | Cricetulus | Colorectal Neoplasms - genetics | Humans | Molecular Targeted Therapy | Receptor, Platelet-Derived Growth Factor beta - genetics | Chemokine CCL5 - antagonists & inhibitors | Leukocytes - immunology | Antibodies, Neutralizing - immunology | Neoplasm Metastasis | Receptors, CCR5 - metabolism | Colorectal Neoplasms - drug therapy | Female | Chemokine CCL5 - metabolism | Colorectal Neoplasms - metabolism | CHO Cells | Receptor, Platelet-Derived Growth Factor beta - metabolism | Amides - pharmacology | Cricetinae | Treatment Outcome | Disease Progression | HT29 Cells | Cell Movement - drug effects | Animals | Leukocytes - drug effects | Cell Proliferation - drug effects | Mice | Colorectal Neoplasms - pathology | Chemokine CCL5 - immunology | Quaternary Ammonium Compounds - pharmacology | Pathogenesis | Liver | Colorectal carcinoma | Colorectal cancer | Antibodies | Vaccines | Metastasis | Kinases | CD45 antigen | Metastases | Receptors | Colon cancer | Rodents | Animal tissues | Colon | Lesions | Growth factors | CCR5 protein | Cytokines | Melanoma | Stroma | Breast cancer | Gene expression | Cervix | Patients | Biopsy | Pancreatic cancer | Laboratory animals | Prostate | Prostate cancer | Chemokines | Tumors | Peritoneum | Cancer | Neutralization
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7. Full Text Functional role of CCL5/RANTES for HCC progression during chronic liver disease
by Mohs, Antje and Kuttkat, Nadine and Reißing, Johanna and Wolfgang Zimmermann, Henning and Sonntag, Roland and Proudfoot, Amanda and Youssef, Sameh A and de Bruin, Alain and Cubero, Francisco Javier and Trautwein, Christian
Journal of Hepatology, ISSN 0168-8278, 2016, Volume 66, Issue 4, pp. 743 - 753
Graphical abstract 
Gastroenterology and Hepatology | HCC | Inflammation | Fibrosis therapy | NFkB signaling | RANTES | INJURY | CANCER | CHEMOKINE-BINDING PROTEIN | HEPATOCELLULAR-CARCINOMA | CCL5 | MICE | CCR5 | CELL | ANGIOGENESIS | EVASIN-4 | RECEPTOR | DELETION | GASTROENTEROLOGY & HEPATOLOGY | Liver Cirrhosis - immunology | Humans | Male | Liver Neoplasms, Experimental - immunology | RNA, Messenger - metabolism | Chemokine CCL5 - antagonists & inhibitors | Chemokine CCL5 - deficiency | Liver Neoplasms - etiology | Receptors, CCR5 - metabolism | Carcinoma, Hepatocellular - genetics | Carcinoma, Hepatocellular - etiology | Carcinoma, Hepatocellular - immunology | Chemokine CCL5 - metabolism | Liver Cirrhosis - etiology | Hepatitis, Chronic - immunology | Liver Neoplasms - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | Liver Neoplasms - immunology | Disease Progression | Liver Neoplasms, Experimental - etiology | Mice, Knockout | Hematopoiesis - immunology | Animals | Chemokine CCL5 - genetics | Hepatitis, Chronic - complications | Liver Cirrhosis - pathology | Mice | Hepatitis, Chronic - genetics | Development and progression | Liver diseases | Index Medicus
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8. Full Text CCL5 as a potential immunotherapeutic target in triple-negative breast cancer
by Lv, Dandan and Zhang, Yan and Kim, Ha-Jeong and Zhang, Lixing and Ma, Xiaojing
Cellular and Molecular Immunology, ISSN 1672-7681, 07/2013, Volume 10, Issue 4, pp. 303 - 310
Breast cancer (BC) is a leading cause of mortality among women in the world. To date, a number of molecules have been established as disease status indicators... 
triple negative breast cancer | myeloid derived suppressor cell | CCL5 | immunotherapy | RHEUMATOID-ARTHRITIS | SYSTEMIC-LUPUS-ERYTHEMATOSUS | CHEMOKINE RANTES | IMMUNOLOGY | MOUSE MAMMARY-TUMOR | ELEVATED EXPRESSION | INTERFERON-GAMMA | RANTES PROMOTER POLYMORPHISM | ALPHA-INDUCED SECRETION | GENETIC RISK-FACTOR | SMOOTH-MUSCLE CELLS | Biomarkers - metabolism | Immunotherapy - methods | Breast Neoplasms - immunology | Humans | Receptor, ErbB-2 - metabolism | Drug Resistance, Neoplasm | Estrogen Receptor alpha - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Chemokine CCL5 - antagonists & inhibitors | Disease Progression | Receptors, Progesterone - antagonists & inhibitors | Receptors, Progesterone - metabolism | Breast Neoplasms - therapy | Animals | Immunotherapy - trends | Estrogen Receptor alpha - metabolism | Female | Models, Animal | Antineoplastic Agents - pharmacology | Receptor, ErbB-2 - antagonists & inhibitors | Chemokine CCL5 - immunology | Review
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9. Full Text Structure-Based Design of Peptidic Inhibitors of the Interaction between CC Chemokine Ligand 5 (CCL5) and Human Neutrophil Peptides 1 (HNP1)
by Wichapong, Kanin and Alard, Jean-Eric and Ortega-Gomez, Almudena and Weber, Christian and Hackeng, Tilman M and Soehnlein, Oliver and Nicolaes, Gerry A. F
Journal of Medicinal Chemistry, ISSN 0022-2623, 05/2016, Volume 59, Issue 9, pp. 4289 - 4301
Protein–protein interactions (PPIs) are receiving increasing interest, much sparked by the realization that they represent druggable targets. Recently, we... 
MOLECULAR-DYNAMICS | CHEMISTRY, MEDICINAL | DOCKING | PROTEIN-PROTEIN INTERACTIONS | MM-PBSA | KINASE INHIBITORS | COAGULATION-FACTOR VIII | SIMULATION | BINDING FREE-ENERGIES | RATIONAL DESIGN | PREDICTION | alpha-Defensins - antagonists & inhibitors | Peptides - chemistry | Monocytes - cytology | Humans | Cell Adhesion | Chemokine CCL5 - antagonists & inhibitors | Peptides - pharmacology | Thermodynamics | Drug Design | Protein Conformation | alpha-Defensins - metabolism | Chemokine CCL5 - metabolism | Dimerization
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10. Full Text Chemokine CCL5/RANTES inhibition reduces myocardial reperfusion injury in atherosclerotic mice
by Braunersreuther, Vincent and Pellieux, Corinne and Pelli, Graziano and Burger, Fabienne and Steffens, Sabine and Montessuit, Christophe and Weber, Christian and Proudfoot, Amanda and Mach, François and Arnaud, Claire
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2009, Volume 48, Issue 4, pp. 789 - 798
Abstract Although beneficial for cardiomyocyte salvage and to limit myocardial damage and cardiac dysfunction, restoration of blood flow after prolonged... 
Cardiovascular | Myocardial ischemia | Inflammation | CCL5/RANTES | Reperfusion injury | Chemokines | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | TISSUE | NEUTROPHILS | DEFICIENT MICE | CELL BIOLOGY | INFARCTION | IN-VIVO | DISEASE | ISCHEMIA-REPERFUSION | RECEPTORS | CCR5 | Atherosclerosis - pathology | Reactive Oxygen Species - metabolism | Humans | Mice, Transgenic | Apolipoproteins E - metabolism | Chemokine CCL5 - antagonists & inhibitors | Myocardial Ischemia - pathology | Myocardial Reperfusion Injury - pathology | Animals | Ischemia | Chemokine CCL5 - metabolism | Chemokines - metabolism | Mice | Leukocytes - metabolism | Troponin I - metabolism | Apoptosis | Cardiology | Apolipoproteins | Coronary heart disease | Analysis | Cardiac patients
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11. Full Text A novel role of hematopoietic CCL5 in promoting triple-negative mammary tumor progression by regulating generation of myeloid-derived suppressor cells
by Zhang, Yan and Lv, Dandan and Kim, Ha-Jeong and Kurt, Robert A and Bu, Wen and Li, Yi and Ma, Xiaojing
Cell Research, ISSN 1001-0602, 03/2013, Volume 23, Issue 3, pp. 394 - 408
CCL5 is a member of the CC chemokine family expressed in a wide array of immune and non-immune cells in response to stress signals. CCL5 expression correlates... 
triple-negative breast cancer | CHEMOKINE RANTES | COLONY-STIMULATING FACTOR | BREAST-CANCER METASTASIS | BONE-MARROW | MACROPHAGE | bone marrow | CELL BIOLOGY | cytotoxic T lymphocyte | immune response | CCL5 | myeloid-derived suppressor cell | DISEASE | mammary tumor | BEARING MICE | EXPRESSION | T-CELLS | TRANSGENIC MICE | Myeloid Cells - cytology | Humans | Cells, Cultured | Antibodies, Neutralizing - pharmacology | Male | T-Lymphocytes, Cytotoxic | Chemokine CCL5 - antagonists & inhibitors | Disease Progression | Mice, Knockout | Mammary Neoplasms, Animal - pathology | Animals | Mammary Neoplasms, Animal - metabolism | Bone Marrow Transplantation | Chemokine CCL5 - genetics | CD8-Positive T-Lymphocytes - metabolism | Myeloid Cells - metabolism | Chemokine CCL5 - metabolism | Mice | Mice, Inbred BALB C | CD11b Antigen - metabolism | Mammary Neoplasms, Animal - genetics | Original
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12. Full Text Peptide Inhibitor of CXCL4–CCL5 Heterodimer Formation, MKEY, Inhibits Experimental Aortic Aneurysm Initiation and Progression
by Iida, Yasunori and Xu, Baohui and Xuan, Haojun and Glover, Keith J and Tanaka, Hiroki and Hu, Xiaolei and Fujimura, Naoki and Wang, Wei and Schultz, Joshua R and Turner, Court R and Dalman, Ronald L
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 04/2013, Volume 33, Issue 4, pp. 718 - 726
OBJECTIVE—Macrophages are critical contributors to abdominal aortic aneurysm (AAA) disease. We examined the ability of MKEY, a peptide inhibitor of CXCL4–CCL5... 
chemokines | mice | CCL5 | abdominal aortic aneurysm | CXCL4 | ATHEROSCLEROTIC LESIONS | PROGENITOR CELLS | RECRUITMENT | WALL | RECEPTOR CCR2 | RANTES | BONE-MARROW | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | INFUSION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | E-DEFICIENT MICE | Aortic Aneurysm, Abdominal - chemically induced | Aortic Aneurysm, Abdominal - prevention & control | Injections, Intravenous | Aortic Aneurysm, Abdominal - immunology | Apolipoproteins E - deficiency | Male | Aorta, Abdominal - drug effects | Chemokine CCL5 - antagonists & inhibitors | Aortic Aneurysm, Abdominal - metabolism | Leukocytes - immunology | Matrix Metalloproteinase 9 - metabolism | Receptors, CCR5 - metabolism | Chemotaxis, Leukocyte - drug effects | Time Factors | Chemokine CCL5 - metabolism | Aorta, Abdominal - pathology | Angiotensin II | Myocytes, Smooth Muscle - drug effects | Aorta, Abdominal - metabolism | Aortic Aneurysm, Abdominal - pathology | Macrophages - immunology | Disease Models, Animal | Matrix Metalloproteinase 2 - metabolism | Mice, Inbred C57BL | Cells, Cultured | Aortic Aneurysm, Abdominal - genetics | Platelet Factor 4 - antagonists & inhibitors | Disease Progression | Mice, Knockout | Aorta, Abdominal - immunology | Animals | Apolipoproteins E - genetics | Myocytes, Smooth Muscle - immunology | Pancreatic Elastase | Leukocytes - drug effects | Macrophages - drug effects | Mice | Oligopeptides - administration & dosage | Platelet Factor 4 - metabolism | Oligopeptides - pharmacology
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13. Full Text Breast cancer cells condition lymphatic endothelial cells within pre-metastatic niches to promote metastasis
by Lee, Esak and Fertig, Elana J and Jin, Kideok and Sukumar, Saraswati and Pandey, Niranjan B and Popel, Aleksander S
Nature Communications, ISSN 2041-1723, 09/2014, Volume 5, Issue 1, p. 4715
Breast cancer metastasis involves lymphatic dissemination in addition to hematogenous spreading. Although stromal lymphatic vessels (LVs) serve as initial... 
EPITHELIAL-MESENCHYMAL TRANSITION | TRANSCRIPTION FACTORS | STAT3 ACTIVATION | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | RESISTANCE | LYMPHANGIOGENESIS | C-JUN | INTERLEUKIN-6 | TUMOR-GROWTH | SIGNAL TRANSDUCER | Neoplasm Transplantation | Interleukin-6 - antagonists & inhibitors | Lymph Nodes - pathology | Cyclohexanes - pharmacology | Humans | Culture Media, Conditioned - pharmacology | Transplantation, Heterologous | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Triple Negative Breast Neoplasms - drug therapy | Vascular Endothelial Growth Factor A - genetics | Chemokine CCL5 - antagonists & inhibitors | Lymphatic Vessels - drug effects | Benzenesulfonates - pharmacology | Lymphatic Vessels - metabolism | MCF-7 Cells | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Triple Negative Breast Neoplasms - pathology | Female | Lymph Nodes - drug effects | Chemokine CCL5 - metabolism | Lung - metabolism | Interleukin-6 - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Gene Expression | Lung - pathology | Aminosalicylic Acids - pharmacology | Human Umbilical Vein Endothelial Cells - drug effects | Interleukin-6 - genetics | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Lymph Nodes - metabolism | Antibodies, Neutralizing - pharmacology | Lymphatic Metastasis | Cell Adhesion - drug effects | Triazoles - pharmacology | Cell Movement - drug effects | Animals | Triple Negative Breast Neoplasms - genetics | Mice, Nude | Triple Negative Breast Neoplasms - metabolism | Lung - drug effects | Lymphatic Vessels - pathology | Chemokine CCL5 - genetics | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | STAT3 Transcription Factor - antagonists & inhibitors
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