Auswahl der wissenschaftlichen Literatur zum Thema „Vegfc“
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Zeitschriftenartikel zum Thema "Vegfc"
Haiko, Paula, Taija Makinen, Salla Keskitalo, Jussi Taipale, Marika J. Karkkainen, Megan E. Baldwin, Steven A. Stacker, Marc G. Achen und Kari Alitalo. „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, Nr. 15 (02.06.2008): 4843–50. http://dx.doi.org/10.1128/mcb.02214-07.
Der volle Inhalt der QuelleEldrid, Charles, Mire Zloh, Constantina Fotinou, Tamas Yelland, Lefan Yu, Filipa Mota, David L. Selwood und Snezana Djordjevic. „VEGFA, B, C: Implications of the C-Terminal Sequence Variations for the Interaction with Neuropilins“. Biomolecules 12, Nr. 3 (26.02.2022): 372. http://dx.doi.org/10.3390/biom12030372.
Der volle Inhalt der QuelleFountzilas, G., N. Angouridakis, R. M. Wirtz, S. Claas, A. Nikolaou und 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, Nr. 18_suppl (20.06.2006): 5538. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.5538.
Der volle Inhalt der QuelleSecker, Genevieve A., und Natasha L. Harvey. „Regulation of VEGFR Signalling in Lymphatic Vascular Development and Disease: An Update“. International Journal of Molecular Sciences 22, Nr. 14 (20.07.2021): 7760. http://dx.doi.org/10.3390/ijms22147760.
Der volle Inhalt der QuelleSanmartin, Elena, Eloisa Jantus-Lewintre, Rafael Sirera, Jose Javier Sanchez, Marta Usó, Sandra Gallach, Ana Blasco et al. „Prognostic value of “angiogenic” risk score in early-stage NSCLC.“ Journal of Clinical Oncology 30, Nr. 15_suppl (20.05.2012): 10594. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10594.
Der volle Inhalt der QuelleJantus-Lewintre, Eloisa, Marta Usó, Elena Sanmartin, Sandra Gallach, Rafael Sirera, Ana Blasco, Cristina Hernando 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, Nr. 15_suppl (20.05.2013): e22147-e22147. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22147.
Der volle Inhalt der QuelleHunter, Stephanie, Braydon Nault, Kingsley Chukwunonso Ugwuagbo, Sujit Maiti und Mousumi Majumder. „Mir526b and Mir655 Promote Tumour Associated Angiogenesis and Lymphangiogenesis in Breast Cancer“. Cancers 11, Nr. 7 (04.07.2019): 938. http://dx.doi.org/10.3390/cancers11070938.
Der volle Inhalt der QuelleMcCarter, Anna L., und Michael T. Dellinger. „Trametinib Inhibits Lymphatic Vessel Invasion of Bone in a Mouse Model of Gorham-Stout Disease“. Journal of Vascular Anomalies 4, Nr. 4 (15.11.2023): e070. http://dx.doi.org/10.1097/jova.0000000000000070.
Der volle Inhalt der QuelleLim, Lillian, Hung Bui, Olivia Farrelly, Jisheng Yang, Li Li, David Enis, Wanshu Ma et al. „Hemostasis stimulates lymphangiogenesis through release and activation of VEGFC“. Blood 134, Nr. 20 (27.09.2019): 1764–75. http://dx.doi.org/10.1182/blood.2019001736.
Der volle Inhalt der QuelleDumond, Aurore, Christopher Montemagno, Valérie Vial, Renaud Grépin und Gilles Pagès. „Anti-Vascular Endothelial Growth Factor C Antibodies Efficiently Inhibit the Growth of Experimental Clear Cell Renal Cell Carcinomas“. Cells 10, Nr. 5 (17.05.2021): 1222. http://dx.doi.org/10.3390/cells10051222.
Der volle Inhalt der QuelleDissertationen zum Thema "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.
Der volle Inhalt der QuelleMedulloblastoma (MB) is the most common and aggressive pediatric brain tumor. Despite aggressive multimodal treatment, resulting in significant side effects, 30% of patients develop resistance and relapse following the appearance of metastases within 5 years. Recurrences cannot be controlled by conventional (radio- and chemotherapy) or targeted (anti-angiogenic, anti-inflammatory, anti-immune checkpoint) treatments. The objective of my thesis is therefore to discover new targets and relevant therapeutic strategies for these patients at diagnosis or after a relapse.MBs are highly vascularized tumors. The phenomenon of resistance is, in part, linked to the development of blood (angiogenesis) and lymphatic (lymphangiogenesis) vessels in the tumor, which constitute the main routes of metastatic dissemination. The lymphatic growth factor, VEGFC, and its receptors/co-receptors are the major players in lymphangiogenesis. In the first part of my thesis, I showed that VEGFC is inversely correlated to MB cell growth and aggressiveness. Indeed, VEGFC decreases the proliferation and migration of MB cells, as well as their ability to form pseudo-vessels in vitro, by an autocrine signalization. Cells resistant to radiotherapy show elevated levels of VEGFC and lose their ability to migrate and form pseudo-vessels. Irradiation reduces the aggressiveness of MB cells by a VEGFC-dependent process. VEGFC-overexpressing cells and radiation-resistant cells form smaller experimental tumors in nude mice. Thus, VEGC appears to be a negative regulator of MB growth. These results pave the way for the development of pro-VEGFC therapies in these cancers.In the second part of my thesis, I correlated the expression of the ELR+CXCL/CXCR1-2 pro-angiogenic and pro-inflammatory signaling pathway to shorter survival in patients with MB. I showed that a novel pharmacological inhibitor (C29) of CXCR1-2 receptors inhibits proliferation, CXCL8/CXCR1-2-dependent migration, invasion and pseudo-vessel formation by susceptible or resistant MB cells to radiotherapy. C29 reduces the growth of experimental MBs in an ex vivo organotypic mouse model and crosses the blood-brain barrier. Thus, targeting CXCR1-2 represents a promising strategy for the treatment of pediatric MB, at first line or at relapse.Key words: pediatric medulloblastoma, VEGFC/VEGFR, CXCR1-2, ELR+CXCL cytokines, targeted therapy, lymphangiogenesis, angiogenesis
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.
Der volle Inhalt der QuelleFerrão, 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/.
Der volle Inhalt der QuelleLymphatic revascularization is a challenge and the establishment of new therapeutic strategies may improve quality of life from those suffering from lymphatic disorders. The objective of this study was to verify the VEGFC treatment capacity in improving lymphatic vascularization in a time-dependent manner in mouse hind limb (HL) after removal of inguinal lymphnode. The left inguinal lymphnode was surgically removed to mimetize pathologies with decreased lymphatic vascularization. Lymphatic vascular density (Vv) and length (Lv) were evaluated by immunohistochemistry followed by stereology after surgery and/or VEGFC treatment. Control group was not manipulated but received saline instead of VEGFC treatment. VEGFC and FLT4 local expression were assessed by qPCR. There was effect of time over Vv and Lv in the SG and significant difference between CG and SG in the three studied regions (proximal, medium and distal region) of the left HL (LHL). The Lv showed significant difference between CG and SG only in the medium region. The Vv and the Lv for TG were higher than the other groups in all regions of LHL. VEGFC and FLT4 gene expression presented time effect in all regions of the LHL for SG and TG. Both VEGFC and FLT4 gene expression presented significant difference between CG and SG, between SG and TG, and between CG and TG. The results show that mice are good experimental models for VEGFC use as therapy for lymphatic revascularization, and VEGFC treatment increased the lymphatic vasculature already after 3 days of lymphatic damage.
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.
Der volle Inhalt der QuelleMatsumura, Kazuyoshi. „Modulation of VEGFR-2-mediated endothelial-cell activity by VEGF-C/VEGFR-3“. Kyoto University, 2003. http://hdl.handle.net/2433/148461.
Der volle Inhalt der QuelleSilva, 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/.
Der volle Inhalt der QuelleIn rodents, increase of vascular permeability, decidual cell transformation, and uterine angiogenesis are crucial events for the success of pregnancy. Vascular endothelial growth factor (VEGF) is a mitogen for endothelial cells and an inducer of angiogenesis. VEGF acts via two tyrosine kinase family receptors: VEGFR1 and VEGFR2. The aim of this study was to investigate using the immunohistochemical method, the spatiotemporal expression of VEGF and its receptors VEGFR1 e VEGFR2 by mouse endometrial cells on days 4 to 8 of pregnancy. On day 4, VEGF, VEGFR1 and VEGFR2 were expressed mostly by the luminal and glandular epithelium. Stromal cells showed a very weak labeling. On days 5-8, VEGF and its receptors showed an increased labeling throughout the mesometrial decidua. The expression of VEGF, VEGFR1, and VEGFR2 were differentially expressed in the mesometrial cells and in the predecidual cells of the antimesometrial decidua. VEGFR1 and VEGF R2 were highly expressed by endothelial cells of the mesometrial sinusoids, and Nk uterine cells.
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.
Der volle Inhalt der QuelleReille-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.
Der volle Inhalt der QuelleInhibiting angiogenesis is an effective strategy of targeting therapy against cancer. In thiscontext, we develop an antiangiogenic strategy consisting in the design and evaluation of compoundsblocking the VEGF/VEGFR interaction. The first approach was the conception of antagonists of theVEGFR1. Starting from a (3-carboxy-2-ureido) thiophene hit, a variety of heterocyclic analogs wasdeveloped. Interesting chemical observations were made during the synthesis, but no optimization ofthe biochemical activity was achieved. The second approach was the design of peptides that bind tothe receptor-recognition surface of the VEGF. Starting from a cyclic peptide known to bind to theVEGF with a sub-micromolar affinity, new peptides and peptidomimetics were developed. Thestrategy was to design simplified and potentially more stable compounds, and to improve at thesame time the VEGF affinity. The interaction of VEGF with these ligands was studied in vitro by ELISAand ITC experiments, as well as X-ray diffraction for the best compound. Moreover, the investigationof the effects of copper and other divalent metals on the VEGF/VEGFR1 interaction was undertaken.Experiments realized in the laboratory and in collaboration showed that metals were able to displacethe VEGF/VEGFR1 interaction and to induce the dimerisation of the domain 2 of the receptor. Metalsare well known to play an important role in angiogenic phenomena, but their specific targets are stilla matter of debate. In this context, this discovery brings new response elements regarding theirmechanisms of action. Therefore, the objectives of this PhD thesis were the development of newantiangiogenic compounds, as well as the understanding of some aspects of the regulation of angiogenesis
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/.
Der volle Inhalt der QuelleHomman, 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.
Der volle Inhalt der QuelleBücher zum Thema "Vegfc"
Fiedler, Lorna R., und Caroline Pellet-Many, Hrsg. VEGF Signaling. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2217-9.
Der volle Inhalt der QuelleFiedler, Lorna, Hrsg. VEGF Signaling. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2917-7.
Der volle Inhalt der QuelleBandello, F. Anti-VEGF. Basel: Karger, 2010.
Den vollen Inhalt der Quelle findenAnti-VEGF. Basel: Karger, 2010.
Den vollen Inhalt der Quelle findenHarmey, Judith H. VEGF and Cancer. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9148-5.
Der volle Inhalt der QuelleHarmey, Judith H. VEGF and cancer. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2004.
Den vollen Inhalt der Quelle findenChristiana, Ruhrberg, Hrsg. VEGF in development. Austin, Tex: Landes Bioscience/Eurekah.com, 2008.
Den vollen Inhalt der Quelle findenH, Harmey Judith, Hrsg. VEGF and cancer. Georgetown, Tex: Landes Bioscience/Eurekah.com ; New York, N.Y. : Kluwer Academic/Plenum Publishers, 2004.
Den vollen Inhalt der Quelle findenDuker, Jay, und Michelle Liang. Anti-VEGF Use in Ophthalmology. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003522577.
Der volle Inhalt der QuelleHastie, Rohan Ferguson. A study of VEGF gene regulation and assessment of the VEGF promoter as a tumour specific promoter in gene therapy. Birmingham: University of Birmingham, 1999.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Vegfc"
Farooqi, Ammad Ahmad, und Ilhan Yaylim. „miRNA Regulation of VEGF/VEGFR Signaling“. In MicroRNA Targeted Cancer Therapy, 309–25. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05134-5_17.
Der volle Inhalt der QuelleEscudier, Bernard, und Laurence Albiges. „Anti-VEGF and VEGFR Monoclonal Antibodies in RCC“. In Renal Cell Carcinoma, 237–52. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1622-1_11.
Der volle Inhalt der QuelleRoden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi und Athanassios Argiris. „New and Promising Targeted Therapies in First and Second-Line Settings“. In Critical Issues in Head and Neck Oncology, 277–96. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_18.
Der volle Inhalt der Quellede Groot, Heink, Vera Schmit-Eilenberger, Janna Kirchhof und Albert J. Augustin. „Angiostatic and Angiogenic Factors“. In Anti-VEGF, 1–3. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320005.
Der volle Inhalt der QuelleSiemerink, Martin J., Albert J. Augustin und Reinier O. Schlingemann. „Mechanisms of Ocular Angiogenesis and Its Molecular Mediators“. In Anti-VEGF, 4–20. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320006.
Der volle Inhalt der QuelleSchmidt-Erfurth, Ursula, Andreas Pollreisz, Christoph Mitsch und Matthias Bolz. „Antivascular Endothelial Growth Factors in Age-Related Macular Degeneration“. In Anti-VEGF, 21–38. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320007.
Der volle Inhalt der QuelleIacono, Pierluigi, Maurizio Battaglia Parodi und Francesco Bandello. „Antivascular Endothelial Growth Factor in Diabetic Retinopathy“. In Anti-VEGF, 39–53. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320008.
Der volle Inhalt der QuelleBuehl, Wolf, Stefan Sacu und Ursula Schmidt-Erfurth. „Retinal Vein Occlusions“. In Anti-VEGF, 54–72. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320009.
Der volle Inhalt der QuelleBattaglia Parodi, Maurizio, Pierluigi Iacono und Francesco Bandello. „Antivascular Endothelial Growth Factor for Choroidal Neovascularization in Pathologic Myopia“. In Anti-VEGF, 73–83. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320010.
Der volle Inhalt der QuelleBattaglia Parodi, Maurizio, Pierluigi Iacono, Frank D. Verbraak und Francesco Bandello. „Antivascular Endothelial Growth Factors for Inflammatory Chorioretinal Disorders“. In Anti-VEGF, 84–95. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320011.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Vegfc"
Odarenko, K. V., O. V. Salomatina, N. F. Salakhutdinov, M. A. Zenkova und 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.
Der volle Inhalt der Quelle„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.
Der volle Inhalt der Quellede La Motte Rouge, Thibault, Roger Mouawad, Eva Comperat, Jean-Christophe Thery, Stephane Vignot, Morgan Roupret, Jean-Philippe Spano und David Khayat. „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.
Der volle Inhalt der QuelleHirata, Hiroshi, Yuji Hinoda, Koji Ueno, Varahram Shahryari, Z. Laura Tabatabai und 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.
Der volle Inhalt der QuelleWang, Jian, und 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.
Der volle Inhalt der QuelleKhayati, Farah, und 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.
Der volle Inhalt der QuelleMittal, Kriti, Henry Koon, Paul Elson, Pierre Triozzi, Afshin Dowlati, Ernest Borden und Brian Rini. „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.
Der volle Inhalt der QuelleTsimafeyeu, Ilya, Lev Demidov und 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.
Der volle Inhalt der QuelleFarkas, Laszlo, Megan Greve, Daniela Farkas, Vita Kraskauskiene und 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.
Der volle Inhalt der QuelleMartinez, Juan-Carlos, Leticia Campo, Maria Val Toledo, Silvia Sacristan und 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.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Vegfc"
Chen, Cheng-Che, und 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, März 2023. http://dx.doi.org/10.37766/inplasy2023.3.0007.
Der volle Inhalt der QuelleMonvoisin, Arnaud. Mechanisms of VEGF Availability in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, Januar 2004. http://dx.doi.org/10.21236/ada428040.
Der volle Inhalt der QuelleMonvoisin, Arnaud. Mechanisms of VEGF Availability in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, Januar 2003. http://dx.doi.org/10.21236/ada414812.
Der volle Inhalt der QuelleIruela-Arispe, Luisa, und Arnaud Movoisin. Mechanisms of VEGF Availability in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, Januar 2005. http://dx.doi.org/10.21236/ada507142.
Der volle Inhalt der QuelleBobykin, Evgenij, Sergej Korotkih, Ol'ga Morozova und Vadim Krohalev. Anti-VEGF Therapy for Macular Diseases: From Theory to Practice (Interactive Electronic Training Manual). SIB-Expertise, Dezember 2022. http://dx.doi.org/10.12731/er0644.15122022.
Der volle Inhalt der QuelleBredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, Juni 2002. http://dx.doi.org/10.21236/ada407270.
Der volle Inhalt der QuelleBredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, Juni 2004. http://dx.doi.org/10.21236/ada427135.
Der volle Inhalt der QuelleBredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, Juni 2003. http://dx.doi.org/10.21236/ada417429.
Der volle Inhalt der QuelleGabhann, Feilim M. Computational Models of Anti-VEGF Therapies in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, Juni 2013. http://dx.doi.org/10.21236/ada582842.
Der volle Inhalt der QuelleContreras, Muricio A. Lymphatic Regeneration within Porous VEGF-C Hydrogels for Secondary Lymphedema. Fort Belvoir, VA: Defense Technical Information Center, Juli 2002. http://dx.doi.org/10.21236/ada410086.
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