Littérature scientifique sur le sujet « Vegfc/vegfr »
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Articles de revues sur le sujet "Vegfc/vegfr"
Haiko, Paula, Taija Makinen, Salla Keskitalo, Jussi Taipale, Marika J. Karkkainen, Megan E. Baldwin, Steven A. Stacker, Marc G. Achen et 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, no 15 (2 juin 2008) : 4843–50. http://dx.doi.org/10.1128/mcb.02214-07.
Texte intégralJantus-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, no 15_suppl (20 mai 2013) : e22147-e22147. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22147.
Texte intégralMorfoisse, Florent, Fabienne De Toni, Jeremy Nigri, Mohsen Hosseini, Audrey Zamora, Florence Tatin, Françoise Pujol et al. « Coordinating Effect of VEGFC and Oleic Acid Participates to Tumor Lymphangiogenesis ». Cancers 13, no 12 (8 juin 2021) : 2851. http://dx.doi.org/10.3390/cancers13122851.
Texte intégralSecker, Genevieve A., et Natasha L. Harvey. « Regulation of VEGFR Signalling in Lymphatic Vascular Development and Disease : An Update ». International Journal of Molecular Sciences 22, no 14 (20 juillet 2021) : 7760. http://dx.doi.org/10.3390/ijms22147760.
Texte intégralZHAO, JIANFENG, YU GENG, HAIRONG HUA, BIYUN CUN, QIANBO CHEN, XIAOTING XI, LIUSHU YANG et YAN LI. « Fenofibrate inhibits the expression of VEGFC and VEGFR-3 in retinal pigmental epithelial cells exposed to hypoxia ». Experimental and Therapeutic Medicine 10, no 4 (21 août 2015) : 1404–12. http://dx.doi.org/10.3892/etm.2015.2697.
Texte intégralVerbiest, Annelies, Benoit Beuselinck, Gabrielle Couchy, Sylvie Job, Aurelien De Reynies, Clément Meiller, Maarten Albersen et al. « Metastatic clear cell renal cell carcinoma : Proangiogenic gene expression and outcome on sunitinib. » Journal of Clinical Oncology 35, no 15_suppl (20 mai 2017) : e16085-e16085. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e16085.
Texte intégralDe Alarcon, Pedro, Manu Gnanamony et Jessica Garcia. « An in Vitro Study on the Role of Angiogenesis in Iron Deficiency Induced Reactive Thrombocytosis ». Blood 132, Supplement 1 (29 novembre 2018) : 2450. http://dx.doi.org/10.1182/blood-2018-99-115378.
Texte intégralBaker, A. F., T. Dragovich, A. Cui, D. Laheru, C. Campen, D. D. Von Hoff et M. Hidalgo. « Plasma IL-6 level and survival of pancreatic cancer patients treated with a VEGFR inhibitor, vatalanib (PTK/ZK) ». Journal of Clinical Oncology 27, no 15_suppl (20 mai 2009) : e15514-e15514. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e15514.
Texte intégralMatas-Céspedes, Alba, Vanina Rodriguez, Susana Kalko, Eva Gine, Elias Campo, Gael Roue, Armando Lopez-Guillermo, Dolors Colomer et Perez-Galan Patricia. « Follicular Dendrytic Cells Deliver Angiogenesis Signaling To Follicular Lymphoma Cells That Is Hampered By The Pan-PI3K Inhibitor NVP-BKM120 ». Blood 122, no 21 (15 novembre 2013) : 3072. http://dx.doi.org/10.1182/blood.v122.21.3072.3072.
Texte intégralWeidenaar, Alida C., Hendrik J. M. de Jonge, Vaclav Fidler, Arja ter Elst, Tiny Meeuwsen, Jenny Douwes, Jessica C. A. Bouma, Karel Hählen, Willem A. Kamps et Evelina S. de Bont. « Addition of PTK787/ZK 222584 Can Lower the Dosage of Amsacrine To Achieve Equal Amounts of AML Cell Death. » Blood 110, no 11 (16 novembre 2007) : 4199. http://dx.doi.org/10.1182/blood.v110.11.4199.4199.
Texte intégralThèses sur le sujet "Vegfc/vegfr"
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.
Texte intégralMedulloblastoma (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
Chan, Tun-Hao, et 詹敦皓. « Lpar1 regulates lymphangiogenesis through Vegfc/Vegfr-3 in zebrafish ». Thesis, 2012. http://ndltd.ncl.edu.tw/handle/77531298483772027583.
Texte intégral國立臺灣大學
動物學研究所
100
Lysophosphatic acid receptor 1 (Lpar1) has been suggested to have some roles in vascular development because of its high expression in endothelial cells (ECs). However, no significant defect in vascular development was observed in lpar1-knockout mice. We have previously demonstrated that knockdown of lpar1 causes craniofacial cartilage distortion and serious edema in zebrafish. Edema was resulted from the defect in lymphangiogenesis, so I intended to further analyze the expression and regulatory mechanism of Lpar1 in lymphangiogenesis during embryonic development. lpar1 was expressed in dorsal aorta where a lymphatic factor, vegfc, was also expressed. Knockdown of lpar1 caused narrowed space between dorsal aorta and posterior caudal vein. Real-time PCR analysis showed that vegfc but not another lymphatic factor lyve-1 like was reduced in lpar1 morphants. Inhibition of cyclooxygenase-2 (Cox2) caused similar defects in lymphangiogenesis as that in the lpar1 morpholino-injected embryos, but it was unable to be rescued by ectopic expression of cox2 at low dosage. From the results, I suggested that Lpar1 may regulate the expression of vegfc and affect the formation of lymphatic vessels, but its regulatory mechanism remains unclear.