@article{Henke.2007,
  abstract = {Nuclear factor kappa B (NF-kappaB) participates in hypertension-induced vascular and target-organ damage. We tested whether or not endothelial cell-specific NF-kappaB suppression would be ameliorative. We generated Cre/lox transgenic mice with endothelial cell-restricted NF-kappaB super-repressor IkappaBalphaDeltaN (Tie-1-DeltaN mice) overexpression. We confirmed cell-specific IkappaBalphaDeltaN expression and reduced NF-kappaB activity after TNF-alpha stimulation in primary endothelial cell culture. To induce hypertension with target-organ damage, we fed mice a high-salt diet and N(omega)-nitro-l-arginine-methyl-ester (L-NAME) and infused angiotensin (Ang) II. This treatment caused a 40-mm Hg blood pressure increase in both Tie-1-DeltaN and control mice. In contrast to control mice, Tie-1-DeltaN mice developed a milder renal injury, reduced inflammation, and less albuminuria. RT-PCR showed significantly reduced expression of the NF-kappaB targets VCAM-1 and ICAM-1, compared with contr},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Henke, N. and Schmidt-Ullrich, R. and Dechend, R. and Park, J. K. and Qadri, F. and Wellner, M. and Obst, M. and Gross, V. and Dietz, R. and Luft, F. C. and Scheidereit, C. and Muller, D. N.},
  biburl = {http://www.bibsonomy.org/bibtex/2fe9b6da17080b89b77fd623f65128cf0/kanefendt},
  interhash = {1d7a9e91c5ca7cb2f5638229c605fa21},
  intrahash = {fe9b6da17080b89b77fd623f65128cf0},
  journal = {Circ.Res.},
  keywords = {& Adhesion Albuminuria Angiotensin Animals Atherosclerosis B Blood C57BL Cardiovascular Cell Cells Chain Chloride Cultured Dietary Diseases Endothelial Ester Expression Factor-alpha Fusion Gene Humans Hypertension I-kappa II III Inbred Inflammation Intercellular Kidney Methyl Mice Models Molecule-1 NF-kappa NG-Nitroarginine Necrosis Nephritis Nitric Organ Oxide Polymerase Pressure Proteins Reaction Receptor Recombinant Regulation Research Reverse Signal Sodium Specificity Synthase TIE-1 Transcriptase Transduction Transgenic Tumor Type Vascular antagonists biosynthesis blood cells complications control etiology genetics inhibitors metabolism physiology physiopathology prevention protein toxicity},
  number = 3,
  pages = {268-276},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Vascular endothelial cell-specific NF-kappaB suppression attenuates hypertension-induced renal damage},
  url = {PM:17585070},
  volume = 101,
  year = 2007
}

@article{Cappuzzo.2007,
  abstract = {The epidermal growth factor receptor (EGFR) plays a key role in cancer development and progression in several human malignancies including non-small cell lung cancer (NSCLC). Several strategies aimed at inhibiting the EGFR have been investigated in the last years, including the use of small tyrosine kinase inhibitors (TKIs) directed against the intracellular domain of the receptor and monoclonal antibodies targeting its extracellular portion. Subgroups of patients who are more likely to respond to TKIs have been identified based on both clinical and biological features. Never-smoking history has emerged as the most relevant clinical characteristic predictive of response to TKIs in NSCLC, while presence of drug-sensitive EGFR mutations and EGFR gene gain represent critical biological variables associated with an improved outcome for patients exposed to these agents. Recent studies have highlighted the existence of biological factors involved in intrinsic and acquired resistance to TKIs,},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Cappuzzo, F. and Toschi, L. and Finocchiaro, G. and Ligorio, C. and Santoro, A.},
  biburl = {http://www.bibsonomy.org/bibtex/277bee5565bfa32594d200c2c9fedca93/kanefendt},
  interhash = {4eaeb753cc74ef92650ea4ea5bc51c7e},
  intrahash = {77bee5565bfa32594d200c2c9fedca93},
  journal = {Int.J.Biol.Markers},
  keywords = {& Antibodies Biological Carcinoma Dosage Drug Epidermal Factor Gene Growth Human Humans Immunohistochemistry Inhibitors Kinase Kinases Lung Markers Monoclonal Mutation Neoplasm Neoplasms Non-Small-Cell Phosphoproteins Predictive Protein Protein-Tyrosine Proteins Proto-Oncogene Quinazolines Receptor Resistance Tests Tyrosine Value analysis antagonists c-akt drug effects erbB-2 erbB-3 genetics identify inhibitors of protein response therapeutic therapy use},
  number = {1 Suppl 4},
  pages = {S10-S23},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Surrogate predictive biomarkers for response to anti-EGFR agents: state of the art and challenges},
  url = {PM:17520577},
  volume = 22,
  year = 2007
}

@article{Folkman.2007,
  abstract = {Angiogenesis--the process of new blood-vessel growth--has an essential role in development, reproduction and repair. However, pathological angiogenesis occurs not only in tumour formation, but also in a range of non-neoplastic diseases that could be classed together as 'angiogenesis-dependent diseases'. By viewing the process of angiogenesis as an 'organizing principle' in biology, intriguing insights into the molecular mechanisms of seemingly unrelated phenomena might be gained. This has important consequences for the clinical use of angiogenesis inhibitors and for drug discovery, not only for optimizing the treatment of cancer, but possibly also for developing therapeutic approaches for various diseases that are otherwise unrelated to each other},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Folkman, J.},
  biburl = {http://www.bibsonomy.org/bibtex/224ae23315709946658083795ddc2c4f5/kanefendt},
  interhash = {189a31ee5f5fc743c6f85c1ba79b53c2},
  intrahash = {24ae23315709946658083795ddc2c4f5},
  journal = {Nat.Rev.Drug Discov.},
  keywords = {Agents Angiogenesis Animals Antineoplastic Blood Endothelium Humans Inhibitors Neoplasms Neovascularization Pathologic Physiologic Platelets RANGE Research drug effects genetics pathology pharmacology physiology therapeutic therapy use},
  number = 4,
  pages = {273-286},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Angiogenesis: an organizing principle for drug discovery?},
  url = {PM:17396134},
  volume = 6,
  year = 2007
}

@article{Juttner.2006,
  abstract = {PURPOSE: Vascular endothelial growth factor (VEGF)-D and its homolog VEGF-C influence lymphangiogenesis through activation of VEGF receptor 3 (VEGFR-3), and have been implicated in lymphatic tumor spread. Nodal dissemination of gastric adenocarcinomas critically determines clinical outcome and therapeutic options of affected patients. Therefore, we analyzed expression and prognostic significance of VEGF-D along with VEGF-C, and VEGFR-3 in gastric adenocarcinomas. MATERIALS AND METHODS: VEGF-C, VEGF-D, and VEGFR-3 were analyzed in 91 R(0)-resected primary gastric adenocarcinomas, corresponding noncancerous gastric mucosa, and lymph node metastases employing immunohistochemistry and/or in situ hybridization. Blood and lymph vessel densities were assessed after staining with CD31 and LYVE-1-specific antibodies. RESULTS: VEGF-D and VEGF-C were detected in 67.0% and 50.5% of gastric cancers, respectively. Healthy gastric mucosa was negative for VEGF-C and in 12.5% positive for VEGF-D. Prese},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Juttner, S. and Wissmann, C. and Jons, T. and Vieth, M. and Hertel, J. and Gretschel, S. and Schlag, P. M. and Kemmner, W. and Hocker, M.},
  biburl = {http://www.bibsonomy.org/bibtex/2ac1d1b6812b2c96f4f5978564cf44933/kanefendt},
  interhash = {7fc6eb5fc72bd09cccbff8435ae692e0},
  intrahash = {ac1d1b6812b2c96f4f5978564cf44933},
  journal = {J.Clin.Oncol.},
  keywords = {80 Adenocarcinoma Adult Aged Antibodies C Cell Chemistry D Disease-Free Endothelial Factor Growth Humans Immunohistochemistry Laboratories Line Lymphatic Messenger Metastasis Middle Neoplasms Prognosis RNA Receptor-3 Research Stomach Survival Tumor Vascular analysis and blood genetics identify methods mortality over supply},
  number = 2,
  pages = {228-240},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Vascular endothelial growth factor-D and its receptor VEGFR-3: two novel independent prognostic markers in gastric adenocarcinoma},
  url = {PM:16344322},
  volume = 24,
  year = 2006
}

@article{Shibuya.2006,
  abstract = {The VEGF/VPF (vascular endothelial growth factor/vascular permeability factor) ligands and receptors are crucial regulators of vasculogenesis, angiogenesis, lymphangiogenesis and vascular permeability in vertebrates. VEGF-A, the prototype VEGF ligand, binds and activates two tyrosine kinase receptors: VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1). VEGFR1, which occurs in transmembrane and soluble forms, negatively regulates vasculogenesis and angiogenesis during early embryogenesis, but it also acts as a positive regulator of angiogenesis and inflammatory responses, playing a role in several human diseases such as rheumatoid arthritis and cancer. The soluble VEGFR1 is overexpressed in placenta in preeclampsia patients. VEGFR2 has critical functions in physiological and pathological angiogenesis through distinct signal transduction pathways regulating proliferation and migration of endothelial cells. VEGFR3, a receptor for the lymphatic growth factors VEGF-C and VEGF-D, but not for VEGF-A, regu},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Shibuya, M. and Claesson-Welsh, L.},
  biburl = {http://www.bibsonomy.org/bibtex/28e3bb24f0d5fe444f2147966afdd05fb/kanefendt},
  interhash = {51dec8f753df90d1459dd94aaddd254f},
  intrahash = {8e3bb24f0d5fe444f2147966afdd05fb},
  journal = {Exp.Cell Res.},
  keywords = {Aging Animals Cell Cells Development Division Embryonic Endothelial Endothelium Factor Growth Human Humans Japan Ligands Lymphangiogenesis Lymphatic Lymphedema Neovascularization Pathologic Physiologic Placenta Receptor-1 Receptor-2 Research Signal System Transduction Tyrosine Vascular Vertebrates cells cytology genetics physiology physiopathology response},
  number = 5,
  pages = {549-560},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Signal transduction by VEGF receptors in regulation of angiogenesis and lymphangiogenesis},
  url = {PM:16336962},
  volume = 312,
  year = 2006
}

@article{Shiojima.2006,
  abstract = {Postnatal growth of the heart is primarily achieved through hypertrophy of individual myocytes. Cardiac growth observed in athletes represents adaptive or physiological hypertrophy, whereas cardiac growth observed in patients with hypertension or valvular heart diseases is called maladaptive or pathological hypertrophy. These two types of hypertrophy are morphologically, functionally, and molecularly distinct from each other. The serine/threonine protein kinase Akt is activated by various extracellular stimuli in a phosphatidylinositol-3 kinase-dependent manner and regulates multiple aspects of cellular functions including survival, growth and metabolism. In this review we will discuss the role of the Akt signaling pathway in the heart, focusing on the regulation of cardiac growth, contractile function, and coronary angiogenesis. How this signaling pathway contributes to the development of physiological/pathological hypertrophy and heart failure will also be discussed},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Shiojima, I. and Walsh, K.},
  biburl = {http://www.bibsonomy.org/bibtex/2c24011977ff0738124791c547dd0d0d9/kanefendt},
  interhash = {c0c1655f4f5361a86bc06dedbc946cc4},
  intrahash = {c24011977ff0738124791c547dd0d0d9},
  journal = {Genes Dev.},
  keywords = {& Adaptation Animals Cardiac Cardiomegaly Cell Contraction Differentiation Diseases Failure Growth Heart Humans Hypertension Myocardial Myocytes Neovascularization Physiologic Physiological Proteins Proto-Oncogene Signal Sports Transduction c-akt cytology development embryology genetics growth metabolism pathology physiology physiopathology protein},
  number = 24,
  pages = {3347-3365},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway},
  url = {PM:17182864},
  volume = 20,
  year = 2006
}

@article{Shibuya.2006b,
  abstract = {Vascular endothelial growth factor (VEGF)-A, a major regulator for angiogenesis, binds and activates two tyrosine kinase receptors, VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1). These receptors regulate physiological as well as pathological angiogenesis. VEGFR2 has strong tyrosine kinase activity, and transduces the major signals for angiogenesis. However, unlike other representative tyrosine kinase receptors which use the Ras pathway, VEGFR2 mostly uses the Phospholipase-Cgamma-Protein kinase-C pathway to activate MAP-kinase and DNA synthesis. VEGFR2 is a direct signal transducer for pathological angiogenesis including cancer and diabetic retinopathy, thus, VEGFR2 itself and the signaling appear to be critical targets for the suppression of these diseases. VEGFR1 plays dual role, a negative role in angiogenesis in the embryo most likely by trapping VEGF-A, and a positive role in adulthood in a tyrosine kinase-dependent manner. VEGFR1 is expressed not only in endothelial cells but also in mac},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Shibuya, M.},
  biburl = {http://www.bibsonomy.org/bibtex/248716170c028a454d03cdde4372bd3f1/kanefendt},
  interhash = {5dbfeeca61a9a56e00e32028444528bd},
  intrahash = {48716170c028a454d03cdde4372bd3f1},
  journal = {J Biochem.Mol.Biol.},
  keywords = {A Animals Atherosclerosis Cells Chemistry Development Dna Embryonic Endothelial Factor Female Growth Human Humans Inflammation Japan Metastasis Mice Neoplasm Neoplasms Neovascularization Pathologic Physiologic Pre-Eclampsia Pregnancy Proteins Receptor-1 Receptor-2 Research Signal Transduction Tyrosine Vascular Viral blood cells genetics metabolism physiology physiopathology protein response supply therapy},
  number = 5,
  pages = {469-478},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Differential roles of vascular endothelial growth factor receptor-1 and receptor-2 in angiogenesis},
  url = {PM:17002866},
  volume = 39,
  year = 2006
}

@article{Carcereny.2006,
  abstract = {Colorectal cancer (CRC) is the second most common cancer in Western Europe. Combinations of oxaliplatin or irinotecan with fluorouracil have increased responses in first-line therapy up to 40%, but prognosis is still poor. Almost 80% of patients will progress during the first year of treatment and usually become refractory to all current therapies, including EGFR inhibitors. The likelihood of achieving a response to cetuximab-based therapy is not related to overt levels of epidermal growth factor receptor (EGFR) expression in the tumor. Whilst other markers of cetuximab activity, such as phosphorylation status of the EGFR, quantification of ligands and polymorphisms in the promoter or in first intronic region, have not been validated, response rate correlates with the intensity of patient skin reaction. Such a relationship is not as clear as with other anti EGFR therapies, such as the EGFR-specific tyrosine kinase inhibitor, gefitinib, where efficacy appears to correlate with mutations},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Carcereny, E. and Maurel, J.},
  biburl = {http://www.bibsonomy.org/bibtex/22241f0587b827c94106b86f8ce995a2c/kanefendt},
  interhash = {ea65e8c26b6e8fc084322c4b1f722e92},
  intrahash = {2241f0587b827c94106b86f8ce995a2c},
  journal = {Rev.Recent Clin.Trials},
  keywords = {& Animals Antibodies Biomarkers Carcinoma Colorectal Drug Epidermal Europe Factor Factors Growth Humans Immunologic Ligands Medical Monoclonal Mutation Neoplasm Neoplasms Oncology Pharmacological Phosphorylation Prognosis Receptor Resistance Tyrosine antagonists genetics inhibitors pharmacology response therapeutic therapy use},
  number = 2,
  pages = {113-118},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Monoclonal antibodies against epidermal growth factor receptor in advanced colorectal carcinoma: clinical efficacy and markers of sensitivity},
  url = {PM:18473962},
  volume = 1,
  year = 2006
}

@article{Cappuzzo.2008,
  abstract = {Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) demonstrated to significantly improve survival of non-small cell lung cancer patients (NSCLC) previously exposed to chemotherapy. Although clinical features, particularly smoking history, help physicians for identifying the sensitive population, a proper patient selection should not preclude to drug target assessment. EGFR mutations or increased EGFR gene copy number assessed by fluorescence in situ hybridization (FISH) identify NSCLC with the highest chance to respond to the therapy. Although indirect comparisons suggest that mutation analysis is the best available technique for identification of responders, survival improvement is not confined to individuals with tumor shrinkage. For patients with metastatic NSCLC, where definitive cure in not achievable, response is probably not the best end-point, since survival improvement observed with TKI included also patients with stable or progressive disease. Data from l},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Cappuzzo, F.},
  biburl = {http://www.bibsonomy.org/bibtex/28c7ec5956d78dd1114bd4d35a3eaeafd/kanefendt},
  interhash = {b510e942ec288dee857484c6fe8aaa9e},
  intrahash = {8c7ec5956d78dd1114bd4d35a3eaeafd},
  journal = {Lung Cancer},
  keywords = {& Analysis Carcinoma Clinical DNA Drug Epidermal Factor Fluorescence Growth Humans Hybridization In Inhibitors Kinase Lung Mutation Mutational Neoplasm Neoplasms Non-Small-Cell Patient Population Protein Receptor Resistance Selection Situ Topic Trials Tyrosine analysis antagonists as drug genetics identify inhibitors protein response therapeutic therapy use},
  number = 2,
  pages = {160-165},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {EGFR FISH versus mutation: different tests, different end-points},
  url = {PM:18367287},
  volume = 60,
  year = 2008
}

@article{Dong.2009,
  abstract = {Hypoxic response element (HRE) offers satisfactory control over expression of hVEGF(165) in cell levels. However, the characteristics of regenerated blood vessels induced by long-term expression of transferred hVEGF(165) under control of HRE in vivo remain unknown. This study aims to investigate the effect of HRE on control of long-term expression of rAAV-delivered hVEGF(165) gene to ischemic myocardium and evaluate characteristics of angiogenesis induced by hVEGF(165) in vivo. Rabbit ischemic heart models were established surgically, rAAV-9HRE-hVEGF(165) was transfected to ischemia hearts subjected to 12 week ischemia. Molecular biological and immunohistochemistry were employed to determine expressions of HIF-1alpha and hVEGF(165). Microvessel densities of CD31(+) and alpha-SMA(+) regenerated vessels were also evaluated. Expressions of both hVEGF(165) mRNA and protein were upregulated following over-expression of endogenous HIF-1alpha early after ischemia, peaked at 4-6 weeks post-MI,},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Dong, H. and Wang, Q. and Zhang, Y. and Jiang, B. and Xu, X. and Zhang, Z.},
  biburl = {http://www.bibsonomy.org/bibtex/2ae12b8b83cbe6601583e2988c0987828/kanefendt},
  interhash = {a213ce39ffcd119483ea58da2ac44929},
  intrahash = {ae12b8b83cbe6601583e2988c0987828},
  journal = {Exp.Biol.Med.(Maywood.)},
  keywords = {1 A Actins Animals Antigens Blood CD31 Dependovirus Elements Endothelial Expression Factor Gene Genetic Growth Heart Human Humans Hypoxia-Inducible Immunohistochemistry Ischemia Myocardial Myocardium Neovascularization Physiologic Rabbits Regulation Research Response Subunit Therapy Transduction Vascular Vessels alpha biosynthesis blood genetics pathology protein response therapy},
  number = 12,
  pages = {1417-1424},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Angiogenesis induced by hVEGF165 gene controlled by hypoxic response elements in rabbit ischemia myocardium},
  url = {PM:19934363},
  volume = 234,
  year = 2009
}

@article{Ebos.2008,
  abstract = {Vascular endothelial growth factor (VEGF) is a potent proangiogenic protein that activates VEGF receptor (VEGFR) tyrosine kinases expressed by vascular endothelial cells. We previously showed that one of these receptors, VEGFR-2, has a truncated soluble form (sVEGFR-2) that can be detected in mouse and human plasma. Because activation of VEGFR-2 plays an important role in tumor angiogenesis, clinical interest in monitoring plasma sVEGFR-2 levels in cancer patients has focused on its potential exploitation as a surrogate biomarker for disease progression as well as assessing efficacy/activity of antiangiogenic drugs, particularly those that target VEGF or VEGFR-2. However, no preclinical studies have been done to study sVEGFR-2 during tumor growth or the mechanisms involved in its modulation. Using spontaneously growing tumors and both localized and metastatic human tumor xenografts, we evaluated the relationship between sVEGFR-2 and tumor burden as well as underlying factors governing },
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Ebos, J. M. and Lee, C. R. and Bogdanovic, E. and Alami, J. and Van, Slyke P. and Francia, G. and Xu, P. and Mutsaers, A. J. and Dumont, D. J. and Kerbel, R. S.},
  biburl = {http://www.bibsonomy.org/bibtex/271956b27a8f21b1b822b52d005ae329f/kanefendt},
  interhash = {e9064ce3c5ea9d32691b0145526d01b9},
  intrahash = {71956b27a8f21b1b822b52d005ae329f},
  journal = {Cancer Res.},
  keywords = {A Adenocarcinoma Adenoviridae Animals BALB Biological Burden C C57BL Cell Cells Cultured Disease Endothelial Experimental Factor Female Genetic Growth HT29 Heterologous Human Humans Inbred Male Mammary Markers Mice Neoplasm Neoplasms Progression Proliferation Prostatic Receptor-2 Research Solubility Transduction Transfection Transgenic Transplantation Tumor Tyrosine Vascular blood cells genetics metabolism methods pathology physiology protein},
  number = 2,
  pages = {521-529},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Vascular endothelial growth factor-mediated decrease in plasma soluble vascular endothelial growth factor receptor-2 levels as a surrogate biomarker for tumor growth},
  url = {PM:18199548},
  volume = 68,
  year = 2008
}

@article{Schneider.2008,
  abstract = {PURPOSE: No biomarkers have been identified to predict outcome with the use of an antiangiogenesis agent for cancer. Vascular endothelial growth factor (VEGF) genetic variability has been associated with altered risk of breast cancer and variable promoter activity. Therefore, we evaluated the association of VEGF genotype with efficacy and toxicity in E2100, a phase III study comparing paclitaxel versus paclitaxel plus bevacizumab as initial chemotherapy for metastatic breast cancer. PATIENTS AND METHODS: DNA was extracted from tumor blocks of patients from E2100. Three hundred sixty-three samples were available to evaluate associations between genotype and outcome. Genotyping was performed for selected polymorphisms in VEGF and VEGF receptor 2. Testing for associations between each polymorphism and efficacy and toxicity was performed. RESULTS: The VEGF-2578 AA genotype was associated with a superior median overall survival (OS) in the combination arm when compared with the alternate ge},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Schneider, B. P. and Wang, M. and Radovich, M. and Sledge, G. W. and Badve, S. and Thor, A. and Flockhart, D. A. and Hancock, B. and Davidson, N. and Gralow, J. and Dickler, M. and Perez, E. A. and Cobleigh, M. and Shenkier, T. and Edgerton, S. and Miller, K. D.},
  biburl = {http://www.bibsonomy.org/bibtex/23674c1605b59b98e071107381fac2b75/kanefendt},
  interhash = {4b2e84e97b68b9c94cd37f38e68a0fa8},
  intrahash = {3674c1605b59b98e071107381fac2b75},
  journal = {J.Clin.Oncol.},
  keywords = {& A Antibodies Antineoplastic Breast Chemotherapy Combined Dna Endothelial Factor Female Genotype Growth Haplotypes Hazards Humans Hypertension Models Monoclonal Neoplasms Nonparametric Nucleotide Paclitaxel Polymorphism Proportional Protocols Rate Receptor-2 Research Retrospective Single Statistics Studies Survival Vascular administration dosage drug genetics methods pathology therapeutic therapy toxicity use},
  number = 28,
  pages = {4672-4678},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Association of vascular endothelial growth factor and vascular endothelial growth factor receptor-2 genetic polymorphisms with outcome in a trial of paclitaxel compared with paclitaxel plus bevacizumab in advanced breast cancer: ECOG 2100},
  url = {PM:18824714},
  volume = 26,
  year = 2008
}

@article{Sawyers.2008,
  abstract = {Genomic technologies offer the promise of a comprehensive understanding of cancer. These technologies are being used to characterize tumours at the molecular level, and several clinical successes have shown that such information can guide the design of drugs targeted to a relevant molecule. One of the main barriers to further progress is identifying the biological indicators, or biomarkers, of cancer that predict who will benefit from a particular targeted therapy},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Sawyers, C. L.},
  biburl = {http://www.bibsonomy.org/bibtex/297f278d43c87e1bf5d59ecfe205b0bdf/kanefendt},
  interhash = {c16a744c0c629dc3f9282b89bdfab4be},
  intrahash = {97f278d43c87e1bf5d59ecfe205b0bdf},
  journal = {Nature},
  keywords = {Biological Human Humans Markers Neoplasms Pharmacogenetics Prognosis Research Tumor analysis classification diagnosis genetics metabolism therapy},
  number = 7187,
  pages = {548-552},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {The cancer biomarker problem},
  url = {PM:18385728},
  volume = 452,
  year = 2008
}

@article{Tammela.2008,
  abstract = {Angiogenesis, the growth of new blood vessels from pre-existing vasculature, is a key process in several pathological conditions, including tumour growth and age-related macular degeneration. Vascular endothelial growth factors (VEGFs) stimulate angiogenesis and lymphangiogenesis by activating VEGF receptor (VEGFR) tyrosine kinases in endothelial cells. VEGFR-3 (also known as FLT-4) is present in all endothelia during development, and in the adult it becomes restricted to the lymphatic endothelium. However, VEGFR-3 is upregulated in the microvasculature of tumours and wounds. Here we demonstrate that VEGFR-3 is highly expressed in angiogenic sprouts, and genetic targeting of VEGFR-3 or blocking of VEGFR-3 signalling with monoclonal antibodies results in decreased sprouting, vascular density, vessel branching and endothelial cell proliferation in mouse angiogenesis models. Stimulation of VEGFR-3 augmented VEGF-induced angiogenesis and sustained angiogenesis even in the presence of VEGFR},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Tammela, T. and Zarkada, G. and Wallgard, E. and Murtomaki, A. and Suchting, S. and Wirzenius, M. and Waltari, M. and Hellstrom, M. and Schomber, T. and Peltonen, R. and Freitas, C. and Duarte, A. and Isoniemi, H. and Laakkonen, P. and Christofori, G. and Yla-Herttuala, S. and Shibuya, M. and Pytowski, B. and Eichmann, A. and Betsholtz, C. and Alitalo, K.},
  biburl = {http://www.bibsonomy.org/bibtex/2b27000713c04489b8399bb1ffbbb30d3/kanefendt},
  interhash = {0075498eb4228e559581212491ea84f0},
  intrahash = {b27000713c04489b8399bb1ffbbb30d3},
  journal = {Nature},
  keywords = {& Adult Angiogenesis Animals Antibodies BALB Blood C Cell Cells Dipeptides Down-Regulation Endothelial Endothelium Expression Factor Factors Female Gene Growth Humans Inbred Inhibitors Laboratories Ligands Line Lymphangiogenesis Mice Monoclonal Neoplasms Neoplastic Neovascularization Notch Pathologic Proliferation Receptor-3 Receptors Regulation Research Signal Transduction Transgenic Tumor Tyrosine Vascular Vessels antagonists blood cells drug effects genetics inhibitors metabolism pharmacology supply therapy},
  number = 7204,
  pages = {656-660},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Blocking VEGFR-3 suppresses angiogenic sprouting and vascular network formation},
  url = {PM:18594512},
  volume = 454,
  year = 2008
}

@article{Simiantonaki.2008,
  abstract = {Adaptation to hypoxia, a universal hallmark of carcinomas, is a critical step for tumor cell survival and growth. One of the principal regulators of hypoxia-responsive pathways is the transcription factor hypoxia-inducible factor-1 alpha (HIF-1 alpha). Currently, it is known that tumoral production of members of the vascular endothelial growth factor (VEGF)-family (VEGFs) may promote tumor growth and progression by acting on carcinoma cells that express the cognate receptors (VEGFRs). However, the influence of hypoxia in the formation of such a tumoral VEGF/VEGFR loop is not completely understood. In the present study we examined the potential existence of a HIF-1 alpha/VEGF/VEGFR autocrine loop on commonly occurring carcinomas. The experiments were performed on five colorectal carcinoma cell lines, one breast (MCF7) and one lung (A549) adenocarcinoma cell line under normoxic and oxygen stress conditions using HIF-1 alpha-EIA, VEGFs-ELISA as well as RT-PCR and immunofluorescence for VE},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Simiantonaki, N. and Jayasinghe, C. and Michel-Schmidt, R. and Peters, K. and Hermanns, M. I. and Kirkpatrick, C. J.},
  biburl = {http://www.bibsonomy.org/bibtex/294c1263be4532fda2056dce70ae83ab4/kanefendt},
  interhash = {4dc9f3c1402a31fa9b63d1d46271568f},
  intrahash = {94c1263be4532fda2056dce70ae83ab4},
  journal = {Int.J.Oncol.},
  keywords = {1 Adenocarcinoma Autocrine Breast C Carcinoma Cell Colorectal Communication Endothelial Expression Factor Gene Growth Human Humans Hypoxia Hypoxia-Inducible Line Lung Neoplasms Neoplastic Oxygen Receptor-1 Receptor-2 Receptor-3 Regulation Subunit Survival Tumor Up-Regulation Vascular alpha cells genetics metabolism pathology physiology protein},
  number = 3,
  pages = {585-592},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Hypoxia-induced epithelial VEGF-C/VEGFR-3 upregulation in carcinoma cell lines},
  url = {PM:18292935},
  volume = 32,
  year = 2008
}

@article{Swendeman.2008,
  abstract = {Vascular endothelial growth factor (VEGF)-A and the VEGF receptors are critical for regulating angiogenesis during development and homeostasis and in pathological conditions, such as cancer and proliferative retinopathies. Most effects of VEGF-A are mediated by the VEGFR2 and its coreceptor, neuropilin (NRP)-1. Here, we show that VEGFR2 is shed from cells by the metalloprotease disintegrin ADAM17, whereas NRP-1 is released by ADAM10. VEGF-A enhances VEGFR2 shedding by ADAM17 but not shedding of NRP-1 by ADAM10. VEGF-A activates ADAM17 via the extracellular signal-regulated kinase (ERK) and mitogen-activated protein kinase pathways, thereby also triggering shedding of other ADAM17 substrates, including tumor necrosis factor alpha, transforming growth factor alpha, heparin-binding epidermal growth factor-like growth factor, and Tie-2. Interestingly, an ADAM17-selective inhibitor shortens the duration of VEGF-A-stimulated ERK phosphorylation in human umbilical vein endothelial cells, prov},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Swendeman, S. and Mendelson, K. and Weskamp, G. and Horiuchi, K. and Deutsch, U. and Scherle, P. and Hooper, A. and Rafii, S. and Blobel, C. P.},
  biburl = {http://www.bibsonomy.org/bibtex/243e4c02a29bd57d4267106b87d1e3b33/kanefendt},
  interhash = {bc8f920d5335e2898ac95ef0db230019},
  intrahash = {43e4c02a29bd57d4267106b87d1e3b33},
  journal = {Circ.Res.},
  keywords = {A ADAM Amyloid Animals Cells Cercopithecus Cos Endothelial Extracellular Factor Factor-alpha Factors Fibroblasts Fusion Growth Human Humans Kinases Knockout MAP Membrane Mice Necrosis Neuropilin-1 Phosphorylation Precursor Protein Proteins Receptor-2 Recombinant Research Secretases Signal Signal-Regulated Swine Time Transduction Transfection Tumor Vascular aethiops cells deficiency enzymology genetics metabolism protein surgery},
  number = 9,
  pages = {916-918},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {VEGF-A stimulates ADAM17-dependent shedding of VEGFR2 and crosstalk between VEGFR2 and ERK signaling},
  url = {PM:18818406},
  volume = 103,
  year = 2008
}

@article{Karpanen.2008,
  abstract = {The lymphatic vasculature is essential for the maintenance of tissue fluid balance, immune surveillance, and adsorption fatty acids in the gut. The lymphatic vessels are also crucially involved in the pathogenesis of diseases such as tumor metastasis, lymphedema, and various inflammatory conditions. Attempts to control or treat these diseases have drawn a lot of interest to lymphatic vascular research during the past few years. Recently, several markers specific for lymphatic endothelium and models for lymphatic vascular research have been characterized, enabling great technical progress in lymphatic vascular biology, and many critical regulators of lymphatic vessel growth have been identified. Despite these significant achievements, our understanding of the lymphatic vessel development and pathogenesis is still rather limited. Several key questions remain to be resolved, including the relative contributions of different pathways targeting lymphatic vasculature, the molecular and cellu},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Karpanen, T. and Alitalo, K.},
  biburl = {http://www.bibsonomy.org/bibtex/25463ed133fd4a573e1e9725dba4bee54/kanefendt},
  interhash = {fddc2a8255c5463b86860788dc0aa07f},
  intrahash = {5463ed133fd4a573e1e9725dba4bee54},
  journal = {Annu.Rev.Pathol.},
  keywords = {Animal Animals Biological Biology Developmental Endothelial Endothelium Expression Factors Gene Growth Humans Laboratories Lymphangiogenesis Lymphatic Lymphedema Markers Mice Models Molecular Regulation Research System Vascular Vessels cytology genetics metabolism methods pathology},
  pages = {367-397},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Molecular biology and pathology of lymphangiogenesis},
  url = {PM:18039141},
  volume = 3,
  year = 2008
}

@article{Park.2008,
  abstract = {Vascular endothelial growth factor-C (VEGF-C) and its receptor, vascular endothelial growth factor receptor-3 (VEGFR-3), have been implicated as important factors in the formation of lymphatic vessels, but its role in osteosarcomas has not yet been fully investigated. This study aims to define the expression of VEGF-C and VEGFR-3 in primary and metastatic osteosarcomas and their relationship to various clinicopathologic parameters. Thirty-three primary osteosarcomas and two pulmonary metastatic samples were immunostained for VEGF-C and VEGFR-3. In addition, VEGF-C and vascular endothelial growth factor-D (VEGF-D) mRNA expression levels in three different human osteosarcoma cell lines and control fibroblasts were evaluated by real-time quantitative polymerase chain reaction (PCR). Both VEGF-C and VEGFR-3 were expressed mainly in the cytoplasm of the tumor cells. Of the 35 patients with osteosarcoma, 16 patients (45.7%) showed strong positive reaction with VEGF-C. Four cases (11.4%) were},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Park, H. R. and Min, K. and Kim, H. S. and Jung, W. W. and Park, Y. K.},
  biburl = {http://www.bibsonomy.org/bibtex/279245c6069a71953b9a702ad2d4030f0/kanefendt},
  interhash = {ba4f65484e4184644eeb26688df1f02f},
  intrahash = {79245c6069a71953b9a702ad2d4030f0},
  journal = {Pathol.Res.Pract.},
  keywords = {Adolescent Adult Aged Bone C Cell Chain Child Cytoplasm D Endothelial Expression Factor Female Gene Growth Human Humans Immunohistochemistry Line Lymphatic Male Messenger Metastasis Middle Neoplasm Neoplasms Neoplastic Osteosarcoma Polymerase RNA Reaction Receptor-3 Regulation Research Up-Regulation Vascular Vessels cells genetics metabolism pathology protein},
  number = 8,
  pages = {575-582},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Expression of vascular endothelial growth factor-C and its receptor in osteosarcomas},
  url = {PM:18440723},
  volume = 204,
  year = 2008
}

@article{Personeni.2008,
  abstract = {PURPOSE: To evaluate the usefulness and the pitfalls inherent to the assessment of the epidermal growth factor receptor (EGFR) gene copy number (GCN) by fluorescence in situ hybridization (FISH) for outcome prediction to cetuximab in metastatic colorectal cancer. The value of testing KRAS mutation status, in addition to EGFR GCN, was also explored. EXPERIMENTAL DESIGN: FISH analysis of 87 metastatic colorectal cancer patients treated with cetuximab was done, recording individual GCN per cell and using different samples per tumor. Performances of published cutoff points and different summaries of EGFR GCN distribution were assessed for response prediction. RESULTS: In our data set, two published cutoff points performed less well than in their training set, yielding positive predictive values and negative predictive values between 40.0% and 48.3% and between 81.0% and 86.5%, respectively. Among summaries of GCN distribution explored, mean and right-tailed distribution of GCN yielded the },
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Personeni, N. and Fieuws, S. and Piessevaux, H. and De, Hertogh G. and De, Schutter J. and Biesmans, B. and De, Roock W. and Capoen, A. and biec Rychter, M. and van Laethem, J. L. and Peeters, M. and Humblet, Y. and Van, Cutsem E. and Tejpar, S.},
  biburl = {http://www.bibsonomy.org/bibtex/22d1ca63c22c53f0332faa42e1895232c/kanefendt},
  interhash = {0e86e74408dfe96c94ab2ceb8026ae21},
  intrahash = {2d1ca63c22c53f0332faa42e1895232c},
  journal = {Clin.Cancer Res.},
  keywords = {80 Adult Aged Antibodies Colorectal Disease-Free Dosage Female Fluorescence Gene Genes Genetic Humans Hybridization In Male Markers Middle Monoclonal Mutation Neoplasms Prognosis Research Situ Survival analysis and drug erbB-1 genetics over response therapeutic therapy use},
  number = 18,
  pages = {5869-5876},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Clinical usefulness of EGFR gene copy number as a predictive marker in colorectal cancer patients treated with cetuximab: a fluorescent in situ hybridization study},
  url = {PM:18794099},
  volume = 14,
  year = 2008
}

@article{Petrova.2008,
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Petrova, T. V. and Bono, P. and Holnthoner, W. and Chesnes, J. and Pytowski, B. and Sihto, H. and Laakkonen, P. and Heikkila, P. and Joensuu, H. and Alitalo, K.},
  biburl = {http://www.bibsonomy.org/bibtex/28f225e24df5de7cf493d587492f3a1cb/kanefendt},
  interhash = {201bc21a7de2dc2625a816faff520ded},
  intrahash = {8f225e24df5de7cf493d587492f3a1cb},
  journal = {Cancer Cell},
  keywords = {Antibodies Antibody Blood Blotting Cell Cells Chain Chemistry Cytometry Endothelial Factor Flow Growth Humans Immunohistochemistry Line Lymphatic Messenger Neoplasms Northern Polymerase RNA Reaction Receptor-3 Reproducibility Results Reverse Separation Specificity Transcriptase Tumor Vascular Vessels Western analysis blood genetics immunology methods of pathology supply},
  number = 6,
  pages = {554-556},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {VEGFR-3 expression is restricted to blood and lymphatic vessels in solid tumors},
  url = {PM:18538738},
  volume = 13,
  year = 2008
}