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Littérature scientifique sur le sujet « Vegfc »

Auteur : Grafiati

Publié le 6 juillet 2024

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Vegfc"

Dormer, Anton, and Gregory Beck. "Evolutionary Analysis of Human Vascular Endothelial Growth Factor, Angiopoietin, and Tyrosine Endothelial Kinase Involved in Angiogenesis and Immunity." In Silico Biology: Journal of Biological Systems Modeling and Multi-Scale Simulation 5, no. 3 (2005): 323–39. https://doi.org/10.3233/isb-00190.

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Human vascular endothelial growth factor (VEGF), angiopoietin (ANG) and tyrosine kinase with immunoglobulin and epidermal growth factor homology domains (TIE)-2 consist of a grouping of proteins that are involved in vascular homeostasis, vascular integrity and angiogenesis. There are nine proteins in the immediate VEGF family: VEGFA, VEGFB, VEGFC, VEGFD, VEGF-3, placental growth factor (PGF), VEGF receptor (VEGFR)-1, VEGFR-2, and VEGFR-1-related. They can be stimulated by cytokines to become involved in immune responses. By using in silico tools, we were able to identify several possible analo

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Haiko, Paula, Taija Makinen, Salla Keskitalo, et al. "Deletion of Vascular Endothelial Growth Factor C (VEGF-C) and VEGF-D Is Not Equivalent to VEGF Receptor 3 Deletion in Mouse Embryos." Molecular and Cellular Biology 28, no. 15 (2008): 4843–50. http://dx.doi.org/10.1128/mcb.02214-07.

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ABSTRACT Lymphatic vessels play an important role in the regulation of tissue fluid balance, immune responses, and fat adsorption and are involved in diseases including lymphedema and tumor metastasis. Vascular endothelial growth factor (VEGF) receptor 3 (VEGFR-3) is necessary for development of the blood vasculature during early embryogenesis, but later, VEGFR-3 expression becomes restricted to the lymphatic vasculature. We analyzed mice deficient in both of the known VEGFR-3 ligands, VEGF-C and VEGF-D. Unlike the Vegfr3 −/− embryos, the Vegfc −/−; Vegfd −/− embryos displayed normal blood vas

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Eldrid, Charles, Mire Zloh, Constantina Fotinou, et al. "VEGFA, B, C: Implications of the C-Terminal Sequence Variations for the Interaction with Neuropilins." Biomolecules 12, no. 3 (2022): 372. http://dx.doi.org/10.3390/biom12030372.

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Vascular endothelial growth factors (VEGFs) are the key regulators of blood and lymphatic vessels’ formation and function. Each of the proteins from the homologous family VEGFA, VEGFB, VEGFC and VEGFD employs a core cysteine-knot structural domain for the specific interaction with one or more of the cognate tyrosine kinase receptors. Additional diversity is exhibited by the involvement of neuropilins–transmembrane co-receptors, whose b1 domain contains the binding site for the C-terminal sequence of VEGFs. Although all relevant isoforms of VEGFs that interact with neuropilins contain the requi

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Fountzilas, G., N. Angouridakis, R. M. Wirtz, S. Claas, A. Nikolaou, and K. T. Kalogeras. "Prognostic value of VEGFC, HER2 and HER3 gene expression in recurrent squamous cell head and neck tumors." Journal of Clinical Oncology 24, no. 18_suppl (2006): 5538. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.5538.

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5538 Background: The main prognostic variables of head and neck squamous cell carcinoma (HNSCC) are the location and size of the tumor and the presence of cervical lymph node metastases. Differential gene expression of members of the HER and VEGF families is a common feature in HNSCC. To elucidate the prognostic value and the interrelation of these factors we performed a detailed gene expression analysis within HNSCC tissue samples Methods: We analyzed fresh frozen tissue from 48 recurrent HNSCC tumors stored at -80oC. RNA was isolated with the RNeasy kit (Qiagen, Inc.), followed by kinetic on

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Karimi, Hanieh, Sarah Lee, Wenqi Xu, et al. "Advances in Molecular Imaging of VEGFRs: Innovations in Imaging and Therapeutics." International Journal of Molecular Sciences 26, no. 11 (2025): 5373. https://doi.org/10.3390/ijms26115373.

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Vascular endothelial growth factor receptors (VEGFRs) are key regulators of angiogenesis, lymphangiogenesis, and vascular permeability, playing essential roles in both physiological and pathological processes. The VEGFR family, including VEGFR-1, VEGFR-2, and VEGFR-3, interacts with structurally related VEGF ligands (VEGFA, VEGFB, VEGFC, VEGFD, and placental growth factor [PlGF]), activating downstream signaling pathways that mediate critical cellular processes, including proliferation, migration, and survival. Dysregulation of VEGFR signaling has been implicated in numerous diseases, such as

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Secker, Genevieve A., and Natasha L. Harvey. "Regulation of VEGFR Signalling in Lymphatic Vascular Development and Disease: An Update." International Journal of Molecular Sciences 22, no. 14 (2021): 7760. http://dx.doi.org/10.3390/ijms22147760.

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The importance of lymphatic vessels in a myriad of human diseases is rapidly gaining recognition; lymphatic vessel dysfunction is a feature of disorders including congenital lymphatic anomalies, primary lymphoedema and obesity, while improved lymphatic vessel function increases the efficacy of immunotherapy for cancer and neurological disease and promotes cardiac repair following myocardial infarction. Understanding how the growth and function of lymphatic vessels is precisely regulated therefore stands to inform the development of novel therapeutics applicable to a wide range of human disease

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Sanmartin, Elena, Eloisa Jantus-Lewintre, Rafael Sirera, et al. "Prognostic value of “angiogenic” risk score in early-stage NSCLC." Journal of Clinical Oncology 30, no. 15_suppl (2012): 10594. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10594.

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10594 Background: Angiogenesis is a key mechanism in tumor growth and dissemination mainly regulated by VEGF family members. We analyze the expression of 11 angiogenic genes in a cohort of resectable NSCLC patients and correlate them with clinico-pathological variables and prognosis. Methods: RNA was obtained from tumor and normal lung specimens from 175 NSCLC patients. RT-PCR was performed to assess the expression of HIF1-A, PIGF, VEGFA, VEGFB, VEGFC, VEGFD, VEGFR1, VEGFR2, VEGFR3, NRP1 and NRP2. Relative expression was normalized by an endogenous gene (GUS) using the Pfaffl formulae. Differe

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Jantus-Lewintre, Eloisa, Marta Usó, Elena Sanmartin, et al. "Ratios between VEGF ligands and receptors in tumor and stroma have impact on the outcome in resectable NSCLC." Journal of Clinical Oncology 31, no. 15_suppl (2013): e22147-e22147. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22147.

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e22147 Background: In tumor angiogenesis there is a complex interplay between endothelial, stromal and tumor cells. Some key regulators of this process are the members of the vascular endothelial growth factor (VEGF) family of ligands and receptors and the neuropilins (NRP). This study analyzes the correlations between the expression of these angiogenic factors in tumor cells and tumor stroma, and their prognostic role in tissue samples from resected non-small cell lung cancer (NSCLC) patients. Methods: Representative tumor and stroma areas from FFPE tissue samples of 125 early-stage NSCLC pat

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Yang, Yi, Weiqiu Lan, Baihong Liu, and Yang Chen. "Abstract 3836: Discovery of a highly potent fully human VEGF nanobody from RenNano transgenic mice that exhibits a superior blocking activity on VEGF function." Cancer Research 85, no. 8_Supplement_1 (2025): 3836. https://doi.org/10.1158/1538-7445.am2025-3836.

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Abstract Background: VEGFA (or VEGF hereafter) is the prototypic member of a family that also includes placental growth factor (PLGF, also known as PGF),VEGFB,VEGFC,VEGFD . VEGFR2 is the major mediator of the physiological and pathological effects of VEGF. VEGFR2 mediates EC proliferation, migration and arterial fate specification [1]. VEGFA monoclonal antibodies have significant therapeutic effects in the treatment of tumors and macular degeneration [2]. In this study, we evaluated a fully human anti-VEGFA mAb generated from our fully human antibody RenNanoTM mice. Methods: Blocking activity

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Hunter, Stephanie, Braydon Nault, Kingsley Chukwunonso Ugwuagbo, Sujit Maiti, and Mousumi Majumder. "Mir526b and Mir655 Promote Tumour Associated Angiogenesis and Lymphangiogenesis in Breast Cancer." Cancers 11, no. 7 (2019): 938. http://dx.doi.org/10.3390/cancers11070938.

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MicroRNAs (miRNAs) are small endogenously produced RNAs, which regulate growth and development, and oncogenic miRNA regulate tumor growth and metastasis. Tumour-associated angiogenesis and lymphangiogenesis are processes involving the release of growth factors from tumour cells into the microenvioronemnt to communicate with endothelial cells to induce vascular propagation. Here, we examined the roles of cyclo-oxygenase (COX)-2 induced miR526b and miR655 in tumour-associated angiogenesis and lymphangiogenesis. Ectopic overexpression of miR526b and miR655 in poorly metastatic estrogen receptor (

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Thèses sur le sujet "Vegfc"

Penco-Campillo, Manon. "Le VEGFC et les récepteurs CXCR1/2 : des cibles pertinentes pour le traitement des médulloblastomes pédiatriques." Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6025.

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Le médulloblastome (MB) est la tumeur pédiatrique cérébrale la plus fréquente et la plus agressive. Malgré un traitement multimodal agressif, entraînant des effets secondaires importants, 30% des patients développent une résistance et rechutent suite à l'apparition de métastases dans les 5 ans. Les récidives ne peuvent être contrôlées par des traitements conventionnels (radio et chimiothérapie) ou ciblés (anti-angiogénique, anti-inflammatoire, anti-point de contrôle immunitaire). L'objectif de ma thèse est donc de découvrir de nouvelles cibles et stratégies thérapeutiques pertinentes pour ces

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Decio, Alessandra Agnese. "The VEGFC/VEGFR3 pathway in the malignancy of ovarian carcinoma." Thesis, Open University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606839.

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Vascular endothelial growth factor C (VEGFC) promotes tumor progression in several tumor types, mainly through the stimulation of lymphangiogenesis and lymphatic metastasis. The expression and biological significance of the VEGFCNEGFR3 pathway in ovarian cancer growth and dissemination has been investigated in this thesis using ovarian carcinoma cell lines and tumor animal models. In patient-derived ovarian carcinoma xenografts (HOC), high levels of soluble VEGFC in ascites and serum were detected, in association with disease progression and tumor burden. Peak VEGFC expression preceded para-ao

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Ferrão, Juliana Shimara Pires. "Tratamento com VEGFC para revascularização linfática em membros pélvicos de camundongos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-08012014-112630/.

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A revascularização linfática é um desafio e o estabelecimento de novas estratégias terapêuticas podem melhorar a qualidade de vida de pessoas que sofrem de distúrbios linfáticos. O objetivo deste estudo foi verificar a capacidade de tratamento com VEGFC exógeno na melhoria da vascularização linfática de uma maneira dependente do tempo em membros pélvicos (MP) de camundongos após a remoção do linfonodo inguinal. O linfonodo inguinal esquerdo foi removido cirurgicamente para mimetizar patologias com diminuição da vascularização linfática. Densidade vascular linfática (Vv) e de comprimento (Lv) f

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Dellinger, Mike. "Contrasting Defects in Lymphangiogenic Remodeling and Lymphangiogenesis Revealed in Angiopoietin-2 Deficient and Vegfc Hemizygous Mice." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/195639.

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Despite recent advances in lymphology, the molecular mechanisms regulating the development of the lymphatic system have not been fully delineated. Here I show that the growth factors Angiopoietin-2 (Ang2) and Vascular endothelial growth factor-c (Vegfc) serve distinct roles in the development of the lymphatic system.Adult Ang2-/- mice exhibit dermal lymphatic hypoplasia, abnormal smooth muscle cell (SMC) coverage of initial lymphatic vessels, and a severe deficiency of collecting lymphatic vessels. To determine whether these abnormalities were due to defects in the remodeling of the lymphati

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Matsumura, Kazuyoshi. "Modulation of VEGFR-2-mediated endothelial-cell activity by VEGF-C/VEGFR-3." Kyoto University, 2003. http://hdl.handle.net/2433/148461.

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Silva, Luciana Oliveira da. "Expressão do fator de crescimento endotelial vascular (VEGF) e seus receptores VEGFR-1 e VEGFR-2 durante o início da gestação em camundongos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-09092008-114452/.

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Em roedores, o aumento da permeabilidade vascular, a transformação decidual, e angiogênese são eventos cruciais para o sucesso da gestação. O fator endotelial vascular (VEGF) é um mitogênico para células endoteliais e um indutor de angiogênese. O VEGF age via dois receptores da família das tirosina quinases: VEGFR1 e VEGFR2. O objetivo deste estudo foi investigar usando o método imunohistoquímico, a expressão espacial e temporal do VEGF e os receptores VEGFR1 e VEGFR2 em células endometriais de camundongo entre o 4º e 8º dias de gestação. No 4º dia de gestação, VEGF, VEGFR1 e VEGFR2 foram expr

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Kranich, Sandra [Verfasser]. "Effekte der Wachstumsfaktoren VEGF-C und VEGF-D und Signaltransduktion des Rezeptors VEGFR-3 in Zellen des zentralen Nervensystems / Sandra Kranich." Kiel : Universitätsbibliothek Kiel, 2009. http://d-nb.info/1019868597/34.

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Reille-Seroussi, Marie. "Système VEGF/VEGFR : conception et évaluation de molécules ciblées et régulation potentielle par les métaux." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05P614/document.

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Dans les thérapies anticancéreuses, les traitements anti-angiogéniques agissant sur l’axe VEGF/VEGFR ont une place importante en clinique. Dans ce contexte, nous avons conçu et évalué l’activité de nouveaux inhibiteurs de l’interaction VEGF/VEGFR. Une première approche a été la conception de molécules antagonistes du VEGFR1. Différents analogues hétérocycliques dérivant d’un composé de type (3-carboxy-2-ureido) thiophène ont été synthétisés. Des réactivités chimiques intéressantes ont été mises en évidence, mais l’activité biochimique de ces molécules ne s’est pas révélée concluante. Une secon

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Olofsson, Birgitta. "Studies of the vascular endothelial growth factors, VEGFs, and their receptors, focusing on VEGF-B /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3633-1/.

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Homman, Ludiye Jihane. "Rôle et expression du facteur lymphangiogénique VEGF-C et de son récepteur VEGFR-3 au cours du développement du cerveau embryonnaire." Paris 6, 2008. http://www.theses.fr/2008PA066052.

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Le VEGF-C a été caractérisé pour son implication dans le développement des vaisseaux lymphatiques via l’activation de son récepteur à activité tyrosine kinase, VEGFR-3. Le VEGF-C liant également les récepteurs Neuropilines exprimés par les cellules neurales, nous avons examiné si les cellules neurales répondaient au VEGF-C et si elles exprimaient le VEGFR-3. J’ai d’abord montré, in vitro, que le VEGF-C stimule la prolifération des précurseurs neuraux exprimant le VEGFR-3 dans bulbe olfactif embryonnaire ainsi que la prolifération et la migration de précurseurs oligodendrocytaires du chiasma op

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Livres sur le sujet "Vegfc"

Fiedler, Lorna R., and Caroline Pellet-Many, eds. VEGF Signaling. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2217-9.

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Fiedler, Lorna, ed. VEGF Signaling. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2917-7.

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Bandello, F. Anti-VEGF. Karger, 2010.

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Harmey, Judith H. VEGF and Cancer. Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9148-5.

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Christiana, Ruhrberg, ed. VEGF in development. Landes Bioscience/Eurekah.com, 2008.

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H, Harmey Judith, ed. VEGF and cancer. Landes Bioscience/Eurekah.com ; New York, N.Y. : Kluwer Academic/Plenum Publishers, 2004.

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Harmey, Judith H. VEGF and cancer. Landes Bioscience/Eurekah.com, 2004.

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Duker, Jay, and Michelle Liang. Anti-VEGF Use in Ophthalmology. CRC Press, 2024. http://dx.doi.org/10.1201/9781003522577.

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Hastie, Rohan Ferguson. A study of VEGF gene regulation and assessment of the VEGF promoter as a tumour specific promoter in gene therapy. University of Birmingham, 1999.

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Hayessen, Clemens. Altersabhängige Expression von VEGF im Hoden und anderen Geweben der Ratte. [s.n.], 2002.

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Chapitres de livres sur le sujet "Vegfc"

Farooqi, Ammad Ahmad, and Ilhan Yaylim. "miRNA Regulation of VEGF/VEGFR Signaling." In MicroRNA Targeted Cancer Therapy. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05134-5_17.

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Escudier, Bernard, and Laurence Albiges. "Anti-VEGF and VEGFR Monoclonal Antibodies in RCC." In Renal Cell Carcinoma. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1622-1_11.

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Roden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi, and Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings." In Critical Issues in Head and Neck Oncology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_18.

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AbstractDeeper understanding of the molecular pathogenesis of malignancies, including head and neck squamous cell carcinoma (HNSCC), has led to the investigation of several novel targeted therapies. These therapeutic approaches may eventually replace or complement existing treatment modalities, such as surgery, radiation therapy, and traditional cytotoxic chemotherapy. Epidermal growth factor receptor (EGFR) inhibitors, and specifically cetuximab, are as of now the only class of targeted agents, excluding immune checkpoint inhibitors, with approval in the treatment of HNSCC. Beyond EGFR inhibi

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de Groot, Heink, Vera Schmit-Eilenberger, Janna Kirchhof, and Albert J. Augustin. "Angiostatic and Angiogenic Factors." In Anti-VEGF. KARGER, 2010. http://dx.doi.org/10.1159/000320005.

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Siemerink, Martin J., Albert J. Augustin, and Reinier O. Schlingemann. "Mechanisms of Ocular Angiogenesis and Its Molecular Mediators." In Anti-VEGF. KARGER, 2010. http://dx.doi.org/10.1159/000320006.

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Schmidt-Erfurth, Ursula, Andreas Pollreisz, Christoph Mitsch, and Matthias Bolz. "Antivascular Endothelial Growth Factors in Age-Related Macular Degeneration." In Anti-VEGF. KARGER, 2010. http://dx.doi.org/10.1159/000320007.

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Iacono, Pierluigi, Maurizio Battaglia Parodi, and Francesco Bandello. "Antivascular Endothelial Growth Factor in Diabetic Retinopathy." In Anti-VEGF. KARGER, 2010. http://dx.doi.org/10.1159/000320008.

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Buehl, Wolf, Stefan Sacu, and Ursula Schmidt-Erfurth. "Retinal Vein Occlusions." In Anti-VEGF. KARGER, 2010. http://dx.doi.org/10.1159/000320009.

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Battaglia Parodi, Maurizio, Pierluigi Iacono, and Francesco Bandello. "Antivascular Endothelial Growth Factor for Choroidal Neovascularization in Pathologic Myopia." In Anti-VEGF. KARGER, 2010. http://dx.doi.org/10.1159/000320010.

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Battaglia Parodi, Maurizio, Pierluigi Iacono, Frank D. Verbraak, and Francesco Bandello. "Antivascular Endothelial Growth Factors for Inflammatory Chorioretinal Disorders." In Anti-VEGF. KARGER, 2010. http://dx.doi.org/10.1159/000320011.

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Actes de conférences sur le sujet "Vegfc"

Odarenko, K. V., O. V. Salomatina, N. F. Salakhutdinov, M. A. Zenkova, and A. V. Markov. "SEARCH FOR REGULATORY GENES AND SMALL-MOLECULAR INHIBITORS OF THE HIGHLY AGGRESSIVE PHENOTYPE OF GLIOBLASTOMA." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-279.

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Four sets of RNA-sequencing data were re-analyzed, and INHBA and VEGFC were found to be novel regulators of the highly aggressive mesenchymal phenotype of glioblastoma; their expression was validated in vitro. In the library of amide derivatives of soloxolone, the compound Jil-46 was identified, which blocked glial‑mesenchymal transition (GMT), inhibited stemness, and induced apoptosis in U87 glioblastoma cells.

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"VEGFC and INHBA as new molecular markers of the glial-mesenchymal transition." In Системная биология и биоинформатика. Федер. исслед. центр Ин-т цитологии и генетики Сиб. отделения Росс. академии наук, 2023. http://dx.doi.org/10.18699/sbb-2023-46.

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de La Motte Rouge, Thibault, Roger Mouawad, Eva Comperat, et al. "Abstract 5138: Expression and circulating levels of VEGFC/VEGFD and their receptor VEGFR2, R3 in renal cell cancer: Relationship with clinicopathological parameters." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5138.

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Hirata, Hiroshi, Yuji Hinoda, Koji Ueno, Varahram Shahryari, Z. Laura Tabatabai, and Rajvir Dahiya. "Abstract 2293: MicroRNA-1826 targets VEGFC, beta-catenin (CTNNB1) and MEK1 (MAP2K1) in human bladder cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2293.

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Wang, Jian, and Shi-Qian Zhang. "VEGF-C, VEGF-D, and VEGFR-3 and their roles in lymphatic metastasis of tumors." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6028987.

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Khayati, Farah, and Samia Mourah. "Abstract 5284: EMMPRIN mediates VEGF activation of VEGFR-2 in melanoma cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5284.

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Mittal, Kriti, Henry Koon, Paul Elson, et al. "Abstract 1184: The effect of dual VEGF/VEGFR inhibition on angiogenic signaling pathways." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1184.

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Tsimafeyeu, Ilya, Lev Demidov, and Nygel Wynn. "Abstract 5157: A role of the FGF-pathway in the VEGF/VEGFR targeting." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5157.

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Farkas, Laszlo, Megan Greve, Daniela Farkas, Vita Kraskauskiene, and Norbert F. Voelkel. "Inhibition Of VEGFr-2 Induces Apoptosis And VEGF Protein Expression In Human Pulmonary Microvascular Endothelial Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5017.

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Martinez, Juan-Carlos, Leticia Campo, Maria Val Toledo, Silvia Sacristan, and Kevin C. Gatter. "Abstract B25: Autocrine action of VEGF/VEGFR pathway in human Glioblastomas in addition to the paracrine angiogenic role." In Abstracts: AACR International Conference on Translational Cancer Medicine--; Mar 21–24, 2010; Amsterdam, The Netherlands. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcme10-b25.

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Rapports d'organisations sur le sujet "Vegfc"

Chen, Cheng-Che, and Hao-En Lin. Survival Benefits and Bleeding Risk of Anti-VEGF Agents for Renal Cell Carcinoma (RCC): A Updated Systematic Review and Meta-Analysis of Phase 2 and 3 Randomized Clinical Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.3.0007.

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Review question / Objective: To investigate the survival benefits (PFS, DFS, OS) and bleeding risk of the anti-VEGF agents compared with placebo or interferon alpha (IFNa) in patients with RCC. Condition being studied: Part 1. The hazard ratio (HR) of the progression-free survival (PFS) and overall survival (OS) of anti-VEGF agents vs. non/placebo for patients with unresectable, advanced, metastatic, renal cell carcinoma (RCC). Part 2. The HR of the disease-free survival (PFS) and OS of anti-VEGF agents vs. non/placebo for patients with post-nephrectomy RCC (adjuvant use). Part 3. The HR of th

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ปทุมราช, สุทธิลักษณ์, ภาวพันธ์ ภัทรโกศล та สัญญา หกพุดซา. ผลของเหงือกปลาหมอดอกขาวต่อการเกิดหลอดเลือดใหม่ และต่อการเติบโตของ เซลล์มะเร็งปากมดลูก ที่ปลูกบนผิวหนังของหนูนู๊ดไมส์ : รายงานฉบับสมบูรณ์โครงการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2011. https://doi.org/10.58837/chula.res.2011.32.

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วัตถุประสงค์ของการศึกษาครั้งนี้เพื่อศึกษาผลของสมุนไพรเหงือกปลาหมอดอกขาวที่สกัดด้วยน้ำต่อการเจริญเติบโตและการเกิดหลอดเลือดใหม่ของมะเร็งปากมดลูก โดยทำการศึกษาในหลอดทดลองเพื่อทดสอบผลการยับยั้งการเจริญของเซลล์มะเร็ง และทำการศึกษาในหนูนูดไมซ์ที่ได้รับการปลูกถ่ายเซลล์มะเร็งปากมดลูกใต้ชั้นผิวหนัง โดยเซลล์มะเร็งปากมดลูกที่ใช้เป็นชนิดที่บรรจุสารชีวะพันธุกรรมของฮิวแมนปาปิลโลมาไวรัส ชนิด 16 (Human papillomavirus type 16, (HPV)-16 DNA) และศึกษาผลของสารสกัดสมุนไพรเหงือกปลาหมอต่อชีวะโมเลกุลที่บ่งชี้การเกิดหลอดเลือดใหม่ของมะเร็ง และการตายของเซลล์มะเร็ง ได้แก่ VEGF และ P53 การศึกษาผลของสารสกัดสมุนไพรเหงือกปลา

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Monvoisin, Arnaud. Mechanisms of VEGF Availability in Prostate Cancer. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada428040.

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Monvoisin, Arnaud. Mechanisms of VEGF Availability in Prostate Cancer. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada414812.

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Iruela-Arispe, Luisa, and Arnaud Movoisin. Mechanisms of VEGF Availability in Prostate Cancer. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada507142.

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Wongpiyabovorn, Jongkonnee, Nattiya Hirankarn, Yingyos Avihingsanon, Tewin Tencomnao, Yong Poovorawan, and Kriangsak Ruchusatsawat. The association between immunogenetics and genetic susceptibility of psoriasis in Thai population. Chulalongkorn University, 2006. https://doi.org/10.58837/chula.res.2006.27.

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Psoriasis is T-cell-mediated skin autoimmunity, required environmental triggers and genetic susceptibility factors to become manifested. Psoriasis is a chronic skin disease characterized by the abnormal hyperproliferation and differentiation of the epidermis, elongated and prominent blood vessels and a thick perivascular lymphocytic infiltrate. Vascular endothelial growth factor (VEGF) gene play important role in pathogenesis of various diseases with angiogenic basis such as breast cancer and autoimmune disease including psoriasis. Many studies analyzed the association of VEGF gene polymorphis

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Bobykin, Evgenij, Sergej Korotkih, Ol'ga Morozova, and Vadim Krohalev. Anti-VEGF Therapy for Macular Diseases: From Theory to Practice (Interactive Electronic Training Manual). SIB-Expertise, 2022. http://dx.doi.org/10.12731/er0644.15122022.

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В работе представлены современные литературные данные, касающиеся антиангиогенной (анти-VEGF) терапии заболеваний макулярной области. Рассмотрены и систематизированы краткие результаты 39 наиболее значимых рандомизированных клинических исследований, посвящённых лечению заболеваний макулы и определивших парадигмы развития современной ретинологии. Приведены собственные отдалённые – в срок наблюдения 60 месяцев – результаты применения анти-VEGF терапии заболеваний макулы в условиях реальной клинической практики, подтверждающие высокую эффективность метода. Работа иллюстрирована краткими описаниям

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Bredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada407270.

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Bredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada427135.

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Bredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada417429.

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