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Artykuły w czasopismach na temat "Vegfc"
Haiko, Paula, Taija Makinen, Salla Keskitalo, Jussi Taipale, Marika J. Karkkainen, Megan E. Baldwin, Steven A. Stacker, Marc G. Achen i 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 (2.06.2008): 4843–50. http://dx.doi.org/10.1128/mcb.02214-07.
Pełny tekst źródłaEldrid, Charles, Mire Zloh, Constantina Fotinou, Tamas Yelland, Lefan Yu, Filipa Mota, David L. Selwood i 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.
Pełny tekst źródłaFountzilas, G., N. Angouridakis, R. M. Wirtz, S. Claas, A. Nikolaou i 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.
Pełny tekst źródłaSecker, Genevieve A., i 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.
Pełny tekst źródłaSanmartin, Elena, Eloisa Jantus-Lewintre, Rafael Sirera, Jose Javier Sanchez, Marta Usó, Sandra Gallach, Ana Blasco i in. "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.
Pełny tekst źródłaJantus-Lewintre, Eloisa, Marta Usó, Elena Sanmartin, Sandra Gallach, Rafael Sirera, Ana Blasco, Cristina Hernando i in. "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.
Pełny tekst źródłaHunter, Stephanie, Braydon Nault, Kingsley Chukwunonso Ugwuagbo, Sujit Maiti i Mousumi Majumder. "Mir526b and Mir655 Promote Tumour Associated Angiogenesis and Lymphangiogenesis in Breast Cancer". Cancers 11, nr 7 (4.07.2019): 938. http://dx.doi.org/10.3390/cancers11070938.
Pełny tekst źródłaMcCarter, Anna L., i 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.
Pełny tekst źródłaLim, Lillian, Hung Bui, Olivia Farrelly, Jisheng Yang, Li Li, David Enis, Wanshu Ma i in. "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.
Pełny tekst źródłaDumond, Aurore, Christopher Montemagno, Valérie Vial, Renaud Grépin i 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.
Pełny tekst źródłaRozprawy doktorskie na temat "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.
Pełny tekst źródłaMedulloblastoma (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.
Pełny tekst źródłaFerrão, 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/.
Pełny tekst źródłaLymphatic 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.
Pełny tekst źródłaMatsumura, Kazuyoshi. "Modulation of VEGFR-2-mediated endothelial-cell activity by VEGF-C/VEGFR-3". Kyoto University, 2003. http://hdl.handle.net/2433/148461.
Pełny tekst źródłaSilva, 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/.
Pełny tekst źródłaIn 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.
Pełny tekst źródłaReille-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.
Pełny tekst źródłaInhibiting 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/.
Pełny tekst źródłaHomman, 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.
Pełny tekst źródłaKsiążki na temat "Vegfc"
Fiedler, Lorna R., i Caroline Pellet-Many, red. VEGF Signaling. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2217-9.
Pełny tekst źródłaFiedler, Lorna, red. VEGF Signaling. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2917-7.
Pełny tekst źródłaBandello, F. Anti-VEGF. Basel: Karger, 2010.
Znajdź pełny tekst źródłaAnti-VEGF. Basel: Karger, 2010.
Znajdź pełny tekst źródłaHarmey, Judith H. VEGF and Cancer. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9148-5.
Pełny tekst źródłaHarmey, Judith H. VEGF and cancer. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2004.
Znajdź pełny tekst źródłaChristiana, Ruhrberg, red. VEGF in development. Austin, Tex: Landes Bioscience/Eurekah.com, 2008.
Znajdź pełny tekst źródłaH, Harmey Judith, red. VEGF and cancer. Georgetown, Tex: Landes Bioscience/Eurekah.com ; New York, N.Y. : Kluwer Academic/Plenum Publishers, 2004.
Znajdź pełny tekst źródłaDuker, Jay, i Michelle Liang. Anti-VEGF Use in Ophthalmology. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003522577.
Pełny tekst źródłaHastie, 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.
Znajdź pełny tekst źródłaCzęści książek na temat "Vegfc"
Farooqi, Ammad Ahmad, i Ilhan Yaylim. "miRNA Regulation of VEGF/VEGFR Signaling". W MicroRNA Targeted Cancer Therapy, 309–25. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05134-5_17.
Pełny tekst źródłaEscudier, Bernard, i Laurence Albiges. "Anti-VEGF and VEGFR Monoclonal Antibodies in RCC". W Renal Cell Carcinoma, 237–52. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1622-1_11.
Pełny tekst źródłaRoden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi i Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings". W 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.
Pełny tekst źródłade Groot, Heink, Vera Schmit-Eilenberger, Janna Kirchhof i Albert J. Augustin. "Angiostatic and Angiogenic Factors". W Anti-VEGF, 1–3. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320005.
Pełny tekst źródłaSiemerink, Martin J., Albert J. Augustin i Reinier O. Schlingemann. "Mechanisms of Ocular Angiogenesis and Its Molecular Mediators". W Anti-VEGF, 4–20. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320006.
Pełny tekst źródłaSchmidt-Erfurth, Ursula, Andreas Pollreisz, Christoph Mitsch i Matthias Bolz. "Antivascular Endothelial Growth Factors in Age-Related Macular Degeneration". W Anti-VEGF, 21–38. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320007.
Pełny tekst źródłaIacono, Pierluigi, Maurizio Battaglia Parodi i Francesco Bandello. "Antivascular Endothelial Growth Factor in Diabetic Retinopathy". W Anti-VEGF, 39–53. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320008.
Pełny tekst źródłaBuehl, Wolf, Stefan Sacu i Ursula Schmidt-Erfurth. "Retinal Vein Occlusions". W Anti-VEGF, 54–72. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320009.
Pełny tekst źródłaBattaglia Parodi, Maurizio, Pierluigi Iacono i Francesco Bandello. "Antivascular Endothelial Growth Factor for Choroidal Neovascularization in Pathologic Myopia". W Anti-VEGF, 73–83. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320010.
Pełny tekst źródłaBattaglia Parodi, Maurizio, Pierluigi Iacono, Frank D. Verbraak i Francesco Bandello. "Antivascular Endothelial Growth Factors for Inflammatory Chorioretinal Disorders". W Anti-VEGF, 84–95. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320011.
Pełny tekst źródłaStreszczenia konferencji na temat "Vegfc"
Odarenko, K. V., O. V. Salomatina, N. F. Salakhutdinov, M. A. Zenkova i A. V. Markov. "SEARCH FOR REGULATORY GENES AND SMALL-MOLECULAR INHIBITORS OF THE HIGHLY AGGRESSIVE PHENOTYPE OF GLIOBLASTOMA". W 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.
Pełny tekst źródła"VEGFC and INHBA as new molecular markers of the glial-mesenchymal transition". W 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.
Pełny tekst źródłade La Motte Rouge, Thibault, Roger Mouawad, Eva Comperat, Jean-Christophe Thery, Stephane Vignot, Morgan Roupret, Jean-Philippe Spano i David Khayat. "Abstract 5138: Expression and circulating levels of VEGFC/VEGFD and their receptor VEGFR2, R3 in renal cell cancer: Relationship with clinicopathological parameters". W 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.
Pełny tekst źródłaHirata, Hiroshi, Yuji Hinoda, Koji Ueno, Varahram Shahryari, Z. Laura Tabatabai i Rajvir Dahiya. "Abstract 2293: MicroRNA-1826 targets VEGFC, beta-catenin (CTNNB1) and MEK1 (MAP2K1) in human bladder cancer." W 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.
Pełny tekst źródłaWang, Jian, i Shi-Qian Zhang. "VEGF-C, VEGF-D, and VEGFR-3 and their roles in lymphatic metastasis of tumors". W 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6028987.
Pełny tekst źródłaKhayati, Farah, i Samia Mourah. "Abstract 5284: EMMPRIN mediates VEGF activation of VEGFR-2 in melanoma cells". W 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.
Pełny tekst źródłaMittal, Kriti, Henry Koon, Paul Elson, Pierre Triozzi, Afshin Dowlati, Ernest Borden i Brian Rini. "Abstract 1184: The effect of dual VEGF/VEGFR inhibition on angiogenic signaling pathways." W 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.
Pełny tekst źródłaTsimafeyeu, Ilya, Lev Demidov i Nygel Wynn. "Abstract 5157: A role of the FGF-pathway in the VEGF/VEGFR targeting". W 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.
Pełny tekst źródłaFarkas, Laszlo, Megan Greve, Daniela Farkas, Vita Kraskauskiene i Norbert F. Voelkel. "Inhibition Of VEGFr-2 Induces Apoptosis And VEGF Protein Expression In Human Pulmonary Microvascular Endothelial Cells". W 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.
Pełny tekst źródłaMartinez, Juan-Carlos, Leticia Campo, Maria Val Toledo, Silvia Sacristan i Kevin C. Gatter. "Abstract B25: Autocrine action of VEGF/VEGFR pathway in human Glioblastomas in addition to the paracrine angiogenic role". W 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.
Pełny tekst źródłaRaporty organizacyjne na temat "Vegfc"
Chen, Cheng-Che, i 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, marzec 2023. http://dx.doi.org/10.37766/inplasy2023.3.0007.
Pełny tekst źródłaMonvoisin, Arnaud. Mechanisms of VEGF Availability in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2004. http://dx.doi.org/10.21236/ada428040.
Pełny tekst źródłaMonvoisin, Arnaud. Mechanisms of VEGF Availability in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2003. http://dx.doi.org/10.21236/ada414812.
Pełny tekst źródłaIruela-Arispe, Luisa, i Arnaud Movoisin. Mechanisms of VEGF Availability in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2005. http://dx.doi.org/10.21236/ada507142.
Pełny tekst źródłaBobykin, Evgenij, Sergej Korotkih, Ol'ga Morozova i Vadim Krohalev. Anti-VEGF Therapy for Macular Diseases: From Theory to Practice (Interactive Electronic Training Manual). SIB-Expertise, grudzień 2022. http://dx.doi.org/10.12731/er0644.15122022.
Pełny tekst źródłaBredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2002. http://dx.doi.org/10.21236/ada407270.
Pełny tekst źródłaBredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2004. http://dx.doi.org/10.21236/ada427135.
Pełny tekst źródłaBredow, Sebastian. Transcriptional Regulation of VEGF Expression in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2003. http://dx.doi.org/10.21236/ada417429.
Pełny tekst źródłaGabhann, Feilim M. Computational Models of Anti-VEGF Therapies in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2013. http://dx.doi.org/10.21236/ada582842.
Pełny tekst źródłaContreras, Muricio A. Lymphatic Regeneration within Porous VEGF-C Hydrogels for Secondary Lymphedema. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2002. http://dx.doi.org/10.21236/ada410086.
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