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1. Vascular growth factors and angiogenesis [Current topics in microbiology and immunology, v. 237]
1999, Current topics in microbiology and immunology, ISBN 3540647317, Volume 237., 189
Vascular endothelium | Growth factors | Neovascularization
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2. Angiogenesis and cardiovascular disease
by Simons, Michael and Ware, J. Anthony
1999, ISBN 9780195112351, xiii, 360
Cardiovascular system | Angiogenesis Factor | Cardiovascular Diseases | Treatment | therapy | Neovascularization | Growth factors | therapeutic use | Diseases
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3. Full Text Thyroid Transcription Factor 1 Reprograms Angiogenic Activities of Secretome
by Wood, Lauren W and Cox, Nicole I and Phelps, Cody A and Lai, Shao-Chiang and Poddar, Arjun and Talbot, Conover and Mu, David
Scientific Reports, ISSN 2045-2322, 02/2016, Volume 6, Issue 1, pp. 19857 - 19857
Through both gain-and loss-of-TTF-1 expression strategies, we show that TTF-1 positively regulates vascular endothelial growth factor (VEGF) and that the VEGF... 
SURVIVAL | MORPHOGENESIS | EPITHELIAL-CELLS | GM-CSF | VEGF | MULTIDISCIPLINARY SCIENCES | LUNG ADENOCARCINOMA | GENE-EXPRESSION | NKX2-1 | CANCER | ENDOTHELIAL GROWTH-FACTOR | Exosomes - metabolism | Angiogenic Proteins - genetics | Neovascularization, Physiologic - drug effects | Thyroid Nuclear Factor 1 | TOR Serine-Threonine Kinases - metabolism | Humans | Lung Neoplasms - metabolism | Culture Media, Conditioned - pharmacology | Lung Neoplasms - pathology | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor Receptor-2 - immunology | Vascular Endothelial Growth Factor A - genetics | Cell Hypoxia | Transcription Factors - secretion | Nuclear Proteins - secretion | Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors | RNA Interference | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Cytokines - genetics | Real-Time Polymerase Chain Reaction | Lung Neoplasms - blood supply | A549 Cells | Promoter Regions, Genetic | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | Cell Survival | Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Indoles - toxicity | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Vascular Endothelial Growth Factor A - analysis | Vascular Endothelial Growth Factor Receptor-1 - metabolism | Blotting, Western | Antibodies - pharmacology | Transcription Factors - metabolism | Up-Regulation - drug effects | Granulocyte-Macrophage Colony-Stimulating Factor - immunology | Pyrroles - toxicity | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Angiogenic Proteins - metabolism | RNA, Small Interfering - metabolism | TOR protein | Statistical analysis | Granulocyte-macrophage colony-stimulating factor | Lung | Lung cancer | Media | Rapamycin | Secretome | Exosomes | Macrophages | Angiogenesis | Hypoxia | Colony-stimulating factor | Vascular endothelial growth factor | Thyroid transcription factor 1 | Thyroid | Index Medicus
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4. Full Text Systemic Effects of Surgery: Quantitative Analysis of Circulating Basic Fibroblast Growth Factor (bFGF), Vascular Endothelial Growth Factor (VEGF) and Transforming Growth Factor Beta (TGF-β) in Patients with Breast Cancer Who Underwent Limited or Extended Surgery
by Curigliano, G and Petit, J Y and Bertolini, F and Colleoni, M and Peruzzotti, G and de Braud, F and Gandini, S and Giraldo, A and Martella, S and Orlando, L and Munzone, E and Pietri, E and Luini, A and Goldhirsch, A
Breast Cancer Research and Treatment, ISSN 0167-6806, 09/2005, Volume 93, Issue 1, pp. 35 - 40
Background. To assess if feature, extent and duration of surgery could influence levels of systemic proangiogenic cytokines vascular endothelial growth factor... 
Medicine & Public Health | angiogenesis | VEGF | Oncology | breast cancer | TGF-β | bFGF | surgery | Angiogenesis | Breast cancer | Surgery | MEDIATES ANGIOGENIC ACTIVITY | THROMBOSPONDIN-1 | SERUM | SURGICAL REMOVAL | TGF-beta | ONCOLOGY | ANGIOSTATIN | RESIDUAL TUMOR | RECURRENCE | INHIBITOR | CARCINOMA | WOUND REPAIR | Breast Neoplasms - surgery | Prospective Studies | Cytokines - metabolism | Humans | Middle Aged | Mastectomy - methods | Neovascularization, Pathologic | Vascular Endothelial Growth Factor A - blood | Vascular Endothelial Growth Factor A - metabolism | Breast Neoplasms - blood supply | Fibroblast Growth Factor 2 - blood | Transforming Growth Factor beta - blood | Breast Neoplasms - metabolism | Breast Neoplasms - blood | Fibroblast Growth Factor 2 - metabolism | Female | Aged | Transforming Growth Factor beta - metabolism | Cytokines - blood | Index Medicus
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5. Full Text GNA11 differentially mediates fibroblast growth factor 2‐ and vascular endothelial growth factor A‐induced cellular responses in human fetoplacental endothelial cells
by Zou, Qing‐yun and Zhao, Ying‐jie and Li, Hua and Wang, Xiang‐zhen and Liu, Ai‐xia and Zhong, Xin‐qi and Yan, Qin and Li, Yan and Zhou, Chi and Zheng, Jing
The Journal of Physiology, ISSN 0022-3751, 06/2018, Volume 596, Issue 12, pp. 2333 - 2344
Fetoplacental vascular growth is critical to fetal growth. Fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are two major... 
growth factor | G‐protein | placental angiogenesis | G-protein | PHYSIOLOGY | HETEROTRIMERIC G-PROTEINS | PERMEABILITY | PHOSPHORYLATION | VEGF | PREECLAMPSIA | SUPPRESSES ANGIOGENIC RESPONSES | PHOSPHOLIPASE C-BETA | NEUROSCIENCES | SMOOTH-MUSCLE | ROLES | ARTERY | Endothelial growth factors | Growth | Analysis | Physiological aspects | Fetus | Fibroblast growth factors | Permeability | G proteins | Protein kinases | Fibroblast growth factor 2 | Fibroblast growth factor | Phosphorylation | AKT1 protein | Thymoma | Pregnancy complications | Extracellular signal-regulated kinase | AKT protein | siRNA | Kinases | Endothelial cells | Blood flow | Cell adhesion & migration | Phospholipase C | Phospholipase | Angiogenesis | Protein kinase | Fibroblasts | Blood pressure | Umbilical cord | Vascular endothelial growth factor | Cell migration | Reproduction and Developmental | Research Paper
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6. Full Text Low temperature plasma induces angiogenic growth factor via up-regulating hypoxia–inducible factor 1α in human dermal fibroblasts
by Cui, Hui Song and Joo, So Young and Lee, Dae Hoon and Yu, Joo Hyang and Jeong, Je Hoon and Kim, June-Bum and Seo, Cheong Hoon
Archives of Biochemistry and Biophysics, ISSN 0003-9861, 09/2017, Volume 630, pp. 9 - 17
Numerous studies on the application of low temperature plasma (LTP) have produced impressive results, including antimicrobial, antitumor, and wound healing... 
Wound healing | Low temperature plasma | HIF1α | Migration | Angiogenic growth factor | Cytokine | IN-VITRO | BIOPHYSICS | HIFl alpha | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROLIFERATION | EXPRESSION | Up-Regulation - drug effects | Neovascularization, Physiologic - drug effects | Dermis - metabolism | Angiogenesis Inducing Agents - metabolism | Humans | Fibroblasts - cytology | Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis | Dermis - cytology | Plasma Gases - pharmacology | Fibroblasts - metabolism | Index Medicus
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7. Full Text Tumor necrosis factor alpha (TNF-α) coordinately regulates the expression of specific matrix metalloproteinases (MMPS) and angiogenic factors during fracture healing
by Lehmann, W and Edgar, C.M and Wang, K and Cho, T-J and Barnes, G.L and Kakar, S and Graves, D.T and Rueger, J.M and Gerstenfeld, L.C and Einhorn, T.A
Bone, ISSN 8756-3282, 2005, Volume 36, Issue 2, pp. 300 - 310
Recent studies from our laboratory demonstrate that TNF-α signaling contributes to the regulation of chondrocyte apoptosis and a lack of TNF-α signaling leads... 
Angiogenesis | Bone repair | Matrix proteins | FAS LIGAND | APOPTOSIS | CHONDROCYTES | angiogenesis | KAPPA-B | matrix proteins | REPAIR | BONE-FORMATION | NUCLEAR-FACTOR | IN-VIVO | ENDOTHELIAL-CELLS | GROWTH | ENDOCRINOLOGY & METABOLISM | bone repair | Chondrocytes - cytology | Matrix Metalloproteinases - genetics | Tumor Necrosis Factor-alpha - genetics | Gene Expression Regulation - physiology | Male | Mice, Transgenic | Tumor Necrosis Factor-alpha - deficiency | Mice, Knockout | Animals | Chondrocytes - physiology | Tumor Necrosis Factor-alpha - physiology | Fracture Healing - physiology | Matrix Metalloproteinases - physiology | Signal Transduction - physiology | Mice | Fracture Healing - genetics | Angiogenic Proteins - metabolism | Angiogenic Proteins - biosynthesis | Cell Survival - physiology | Chondrocytes - metabolism | Matrix Metalloproteinases - biosynthesis | Surgery, Plastic | Cell research | Tumor necrosis factor | Analysis | Genetic research | Ribonuclease | Vascular endothelial growth factor | Aspartic proteinases | Tumors | Endothelium | Index Medicus
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8. Full Text Cotransfection of vascular endothelial growth factor-A and platelet-derived growth factor-B via recombinant adeno-associated virus resolves chronic ischemic malperfusion: Role of vessel maturation
by Kupatt, Christian and Hinkel, Rabea and Pfosser, Achim and El-Aouni, Chiraz and Wuchrer, Alexander and Fritz, Andrea and Globisch, Franziska and Thormann, Michael and Horstkotte, Jan and Lebherz, Corinna and Thein, Eckart and Banfi, Andrea and Boekstegers, Peter
Journal of the American College of Cardiology, ISSN 0735-1097, 07/2010, Volume 56, Issue 5, pp. 414 - 422
Objectives: We set out to investigate the ability of cardiotropic adeno-associated viral vector (AAV2.9 = recombinant adeno-associated virus [rAAV]) to induce... 
gene therapy | angiogenesis | pericytes | arteriogenesis | CARDIAC & CARDIOVASCULAR SYSTEMS | VEGF | FEMORAL-ARTERY OCCLUSION | MYOCARDIAL-ISCHEMIA | BLOOD-FLOW | ANGIOGENIC GENE-THERAPY | STIMULATES ANGIOGENESIS | ADULT NEOVASCULARIZATION | HINDLIMB ISCHEMIA | NITRIC-OXIDE | RABBIT | Gene Transfer Techniques | Rabbits | Proto-Oncogene Proteins c-sis - genetics | Dependovirus - metabolism | Blood Vessels - pathology | Vascular Endothelial Growth Factor A - therapeutic use | Ischemia - therapy | Myocardium - pathology | Genetic Techniques | Vascular Endothelial Growth Factor A - genetics | Animals | Transfection | Swine | Proto-Oncogene Proteins c-sis - therapeutic use | Genetic Vectors | Neovascularization, Physiologic | Genetic Therapy - methods | Heart | Clinical trials | Collateral | Experiments | Catheters | Proteins | Polymerase chain reaction | Angiogenesis | Ischemia | Plasmids | Fixed rates | Laboratory animals | Vascular endothelial growth factor | Drug dosages | Veins & arteries | Index Medicus | Abridged Index Medicus
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9. Full Text Vascular endothelial growth factor-mediated decrease in plasma soluble vascular endothelial growth factor receptor-2 levels as a surrogate biomarker for tumor growth
by Ebos, John M. L and Lee, Christina R and Bogdanovic, Elena and Alami, Jennifer and Van Slyke, Paul and Francia, Giulio and Xu, Ping and Mutsaers, Anthony J and Dumont, Daniel J and Kerbel, Robert S
Cancer Research, ISSN 0008-5472, 01/2008, Volume 68, Issue 2, pp. 521 - 529
Vascular endothelial growth factor (VEGF) is a potent proangiogenic protein that activates VEGF receptor (VEGFR) tyrosine kinases expressed by,vascular... 
ONCOLOGY | METASTATIC BREAST-CANCER | IN-VIVO | VEGF RECEPTOR-1 | SERUM | LEUKEMIA | EXPRESSION | RENAL-CELL CARCINOMA | ANGIOGENIC FACTORS | MYELODYSPLASTIC SYNDROMES | ANTITUMOR EFFICACY | Neoplasm Transplantation | Prostatic Neoplasms - metabolism | Adenocarcinoma - pathology | Adenoviridae | Cell Proliferation | Humans | Male | Transplantation, Heterologous | Mammary Neoplasms, Experimental - metabolism | Vascular Endothelial Growth Factor A - genetics | Mammary Neoplasms, Experimental - genetics | Adenocarcinoma - metabolism | Prostatic Neoplasms - genetics | Mammary Neoplasms, Experimental - pathology | Female | Tumor Burden - genetics | Adenocarcinoma - genetics | Tumor Cells, Cultured | Prostatic Neoplasms - pathology | Transduction, Genetic | Mice, Inbred C57BL | Solubility | Vascular Endothelial Growth Factor Receptor-2 - blood | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Mice, Transgenic | Biomarkers, Tumor - blood | HT29 Cells | Animals | Mice | Mice, Inbred BALB C | Vascular Endothelial Growth Factor A - physiology | Index Medicus
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10. Full Text Macrophages Control Vascular Stem/Progenitor Cell Plasticity Through Tumor Necrosis Factor-α–Mediated Nuclear Factor-κB Activation
by Wong, Mei Mei and Chen, Yikuan and Margariti, Andriani and Winkler, Bernhard and Campagnolo, Paola and Potter, Claire and Hu, Yanhua and Xu, Qingbo
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 03/2014, Volume 34, Issue 3, pp. 635 - 643
OBJECTIVE—Vascular lineage differentiation of stem/progenitor cells can contribute to both tissue repair and exacerbation of vascular diseases such as in vein... 
Tumor necrosis factor-alpha | Vascular smooth muscle | Macrophages | Endothelial cells | Stem cells | PROGENITOR CELLS | stem cells | endothelial cells | vascular smooth muscle | ANGIOGENESIS | ATHEROSCLEROSIS | tumor necrosis factor-alpha | PATHOGENESIS | macrophages | EMBRYONIC STEM-CELLS | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | VEIN BYPASS GRAFTS | MICE | TNF-ALPHA | DIFFERENTIATION | HEMATOLOGY | Endothelium, Vascular - cytology | Neovascularization, Physiologic - drug effects | Antigens, CD - biosynthesis | Tumor Necrosis Factor-alpha - genetics | Veins - transplantation | Culture Media, Conditioned - pharmacology | NF-kappa B - metabolism | Tumor Necrosis Factor-alpha - deficiency | Antigens, CD - genetics | Cadherins - biosynthesis | Receptors, Tumor Necrosis Factor, Type I - drug effects | Thrombophilia - etiology | Tissue Scaffolds | RNA Interference | Nitric Oxide Synthase Type III - physiology | Cadherins - genetics | Myocytes, Smooth Muscle - drug effects | Myocytes, Smooth Muscle - cytology | Angiogenic Proteins - pharmacology | Adult Stem Cells - drug effects | Gene Expression Regulation, Developmental - physiology | Cell Line | Promoter Regions, Genetic | Adult Stem Cells - cytology | Signal Transduction | Thrombophilia - physiopathology | Macrophages, Peritoneal - physiology | Mice, Inbred C57BL | RNA, Small Interfering - pharmacology | Gene Expression Regulation, Developmental - drug effects | Radiation Chimera | Recombinant Proteins - pharmacology | Macrophages, Peritoneal - secretion | Muscle, Smooth, Vascular - cytology | Mice, Knockout | Cell Lineage | Tumor Necrosis Factor-alpha - pharmacology | Animals | Interleukin-6 - pharmacology | Transcription Factor RelA - metabolism | Endothelial Cells - cytology | Receptors, Tumor Necrosis Factor, Type I - physiology | Neointima - pathology | Tumor Necrosis Factor-alpha - physiology | Mice | Apoptosis | Endothelial Cells - drug effects | Index Medicus
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11. Full Text Overcoming evasive resistance from vascular endothelial growth factor a inhibition in sarcomas by genetic or pharmacologic targeting of hypoxia‐inducible factor 1α
by Kim, Yeo‐Jung and Lee, Hae‐June and Kim, Tae‐Min and Eisinger‐Mathason, T.S. Karin and Zhang, Alexia Y and Schmidt, Benjamin and Karl, Daniel L and Nakazawa, Michael S and Park, Peter J and Simon, M. Celeste and Yoon, Sam S
International Journal of Cancer, ISSN 0020-7136, 01/2013, Volume 132, Issue 1, pp. 29 - 41
Increased levels of hypoxia and hypoxia‐inducible factor 1α (HIF‐1α) in human sarcomas correlate with tumor progression and radiation resistance. Prolonged... 
hypoxia | HIF‐1α | sarcomas | VEGF‐A | HIF-1α | VEGF-A | ACTIVATION | HIF-1 alpha | METASTASIS | RANDOMIZED-TRIAL | TUMOR ANGIOGENESIS | CANCER-THERAPY | ONCOLOGY | MOUSE MODEL | ELECTRON-BEAM RADIOTHERAPY | ANTI-ANGIOGENIC THERAPY | UP-REGULATION | SOFT-TISSUE SARCOMA | Genetic Therapy | Cell Hypoxia - physiology | Apoptosis - drug effects | Carbonic Anhydrases - genetics | Humans | Apoptosis - genetics | Hypoxia-Inducible Factor 1, alpha Subunit - antagonists & inhibitors | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Vascular Endothelial Growth Factor A - genetics | Sarcoma - therapy | Bevacizumab | Carbonic Anhydrases - metabolism | DNA-Binding Proteins - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Antibodies, Monoclonal, Humanized - pharmacology | Antigens, Neoplasm - metabolism | Sarcoma - genetics | Carbonic Anhydrase IX | Antigens, Neoplasm - genetics | Cell Line | DNA-Binding Proteins - antagonists & inhibitors | Endothelial Cells - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Antibodies, Monoclonal - pharmacology | DNA-Binding Proteins - genetics | Sarcoma - pathology | Sarcoma - metabolism | Animals | Cell Line, Tumor | Mice | Endothelial Cells - pathology | Doxorubicin - pharmacology | Endothelial Cells - drug effects | Index Medicus | Cancer Cell Biology
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12. Full Text Diagnostic Accuracy of Placental Growth Factor in Women With Suspected Preeclampsia: A Prospective Multicenter Study
by Chappell, Lucy C and Duckworth, Suzy and Seed, Paul T and Griffin, Melanie and Myers, Jenny and Mackillop, Lucy and Simpson, Nigel and Waugh, Jason and Anumba, Dilly and Kenny, Louise C and Redman, Christopher W.G and Shennan, Andrew H
Circulation, ISSN 0009-7322, 11/2013, Volume 128, Issue 19, pp. 2121 - 2131
BACKGROUND—Hypertensive disorders of pregnancy are a major contributor to death and disability for pregnant women and their infants. The diagnosis of... 
diagnosis | angiogenesis inducers | hypertension | pregnancy | REVIEWS | TESTS | CARDIAC & CARDIOVASCULAR SYSTEMS | RISK | ANGIOGENIC FACTORS | PREDICTION | PERIPHERAL VASCULAR DISEASE | COMPLICATIONS | OUTCOMES | Pre-Eclampsia - epidemiology | Predictive Value of Tests | Reproducibility of Results | Prospective Studies | Follow-Up Studies | Humans | Risk Factors | Biomarkers - blood | Chemistry, Clinical - standards | Pregnancy | Pregnancy Proteins - blood | Pre-Eclampsia - blood | Sensitivity and Specificity | Placenta Growth Factor | Adult | Female | Pre-Eclampsia - diagnosis | Physiological aspects | Research | Diagnosis | Growth factors | Preeclampsia | Index Medicus | Abridged Index Medicus
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13. Full Text Cell Type–Specific Regulation of Angiogenic Growth Factor Gene Expression and Induction of Angiogenesis in Nonischemic Tissue by a Constitutively Active Form of Hypoxia-Inducible Factor 1
by Kelly, Brian D and Hackett, Sean F and Hirota, Kiichi and Oshima, Yuji and Cai, Zheqing and Berg-Dixon, Shannon and Rowan, Ashley and Yan, Zhijiang and Campochiaro, Peter A and Semenza, Gregg L
Circulation Research: Journal of the American Heart Association, ISSN 0009-7330, 11/2003, Volume 93, Issue 11, pp. 1074 - 1081
ABSTRACT—Understanding molecular mechanisms regulating angiogenesis may lead to novel therapies for ischemic disorders. Hypoxia-inducible factor 1 (HIF-1)... 
Gene therapy | Angiogenesis | Hypoxia | FACTOR VEGF | hypoxia | HIF-1-ALPHA/VP16 HYBRID | CARDIAC & CARDIOVASCULAR SYSTEMS | angiogenesis | HYDROXYLATION | gene therapy | MODEL | RETINAL NEOVASCULARIZATION | FACTOR 1-ALPHA | IN-VIVO | HINDLIMB ISCHEMIA | PERIPHERAL VASCULAR DISEASE | MICE | HEMATOLOGY | HIF-ALPHA | Angiogenic Proteins - genetics | Neovascularization, Physiologic - drug effects | Cell Hypoxia - physiology | Eye - blood supply | Angiopoietin-2 - genetics | Humans | Pregnancy Proteins - genetics | Male | Pregnancy Proteins - metabolism | Stem Cells - cytology | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | RNA, Messenger - metabolism | Stem Cells - metabolism | Vascular Endothelial Growth Factor A - genetics | Angiopoietin-2 - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit | Genes, Dominant | Transcription Factors - pharmacology | Adenoviridae - genetics | Eye - drug effects | Fibroblasts - metabolism | Transcription Factors - physiology | Proto-Oncogene Proteins c-sis - genetics | Myocytes, Cardiac - cytology | Proto-Oncogene Proteins c-sis - metabolism | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation - physiology | Rats | Transcription Factors - genetics | Gene Expression Regulation - drug effects | Angiopoietin-1 - genetics | Neovascularization, Physiologic - physiology | Animals | Myocytes, Cardiac - drug effects | Fibroblasts - drug effects | Myocytes, Cardiac - metabolism | Placenta Growth Factor | Fibroblasts - cytology | Mice | Angiogenic Proteins - metabolism | Index Medicus
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14. Full Text The growth and aggressive behavior of human osteosarcoma is regulated by a CaMKII-controlled autocrine VEGF signaling mechanism
by Daft, Paul G and Yang, Yang and Napierala, Dobrawa and Zayzafoon, Majd
PLoS ONE, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, pp. e0121568 - e0121568
Osteosarcoma (OS) is a hyperproliferative malignant tumor that requires a high vascular density to maintain its large volume. Vascular Endothelial Growth... 
BREAST-CANCER | SUPPRESSES TUMOR-GROWTH | IN-VITRO | OSTEOBLAST DIFFERENTIATION | MULTIDISCIPLINARY SCIENCES | PROSTATE-CANCER | FACTOR EXPRESSION | CELL-CYCLE ARREST | INDUCIBLE FACTOR-1 | ANGIOGENIC FACTORS | PROTEIN-KINASE-II | Transcription Factor AP-1 - genetics | Humans | Transcriptional Activation - drug effects | Male | Peptides, Cyclic - pharmacology | Transplantation, Heterologous | Autocrine Communication - drug effects | Endothelial Growth Factors - pharmacology | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Bone Neoplasms - pathology | Transcription Factor AP-1 - metabolism | Bone Neoplasms - metabolism | Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors | RNA Interference | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Transcription, Genetic | Vascular Endothelial Growth Factor A - pharmacology | Osteosarcoma - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Neoplasm Invasiveness | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Sulfonamides - pharmacology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Animals | Signal Transduction - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Benzylamines - pharmacology | Osteosarcoma - pathology | RNA, Small Interfering - metabolism | Osteosarcoma | Physiological aspects | Development and progression | Genetic aspects | Research | Vascular endothelial growth factor | Protein kinases | Therapy | Chromatin | Transcription factors | Immunoprecipitation | Transcription | Calcium | Paracrine signalling | Kinases | Proteins | Angiogenesis | Biomedical materials | Rodents | Calcium-binding protein | Biocompatibility | Inhibition | Autocrine signalling | Growth factors | Calmodulin | Calcium (intracellular) | Aggressive behavior | Secretion | Tumor cells | Activator protein 1 | Pharmacology | Tumorigenicity | Gene expression | Vascular endothelial growth factor receptors | Inhibitors | Human behavior | Calcium ions | Ca2+/calmodulin-dependent protein kinase II | Tumors | Index Medicus
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15.