Bibliografías temáticas / Vegfc

Literatura académica sobre el tema "Vegfc"

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Publicado: 6 de julio de 2024

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Artículos de revistas sobre el tema "Vegfc":

Haiko, Paula, Taija Makinen, Salla Keskitalo, Jussi Taipale, Marika J. Karkkainen, Megan E. Baldwin, Steven A. Stacker, Marc G. Achen y 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, n.º 15 (2 de junio de 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 vasculature after embryonic day 9.5. Deletion of Vegfr3 in the epiblast, using keratin 19 (K19) Cre, resulted in a phenotype identical to that of the Vegfr3 −/− embryos, suggesting that this phenotype is due to defects in the embryo proper and not in placental development. Interestingly, the Vegfr3 neo hypomorphic mutant mice carrying the neomycin cassette between exons 1 and 2 showed defective lymphatic development. Overexpression of human or mouse VEGF-D in the skin, under the K14 promoter, rescued the lymphatic hypoplasia of the Vegfc +/− mice in the K14-VEGF-D; Vegfc +/− compound mice, suggesting that VEGF-D is functionally redundant with VEGF-C in the stimulation of developmental lymphangiogenesis. Our results suggest VEGF-C- and VEGF-D-independent functions for VEGFR-3 in the early embryo.

Eldrid, Charles, Mire Zloh, Constantina Fotinou, Tamas Yelland, Lefan Yu, Filipa Mota, David L. Selwood y Snezana Djordjevic. "VEGFA, B, C: Implications of the C-Terminal Sequence Variations for the Interaction with Neuropilins". Biomolecules 12, n.º 3 (26 de febrero de 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 required C-terminal Arg residue, there is selectivity of neuropilins and VEGF receptors for the VEGF proteins, which is reflected in the physiological roles that they mediate. To decipher the contribution made by the C-terminal sequences of the individual VEGF proteins to that functional differentiation, we determined structures of molecular complexes of neuropilins and VEGF-derived peptides and examined binding interactions for all neuropilin-VEGF pairs experimentally and computationally. While X-ray crystal structures and ligand-binding experiments highlighted similarities between the ligands, the molecular dynamics simulations uncovered conformational preferences of VEGF-derived peptides beyond the C-terminal arginine that contribute to the ligand selectivity of neuropilins. The implications for the design of the selective antagonists of neuropilins’ functions are discussed.

Fountzilas, G., N. Angouridakis, R. M. Wirtz, S. Claas, A. Nikolaou y 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, n.º 18_suppl (20 de junio de 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 one-step RT-PCR for the expression of 8 candidate genes (EGFR, HER2, HER3, HER4, VEGFA, VEGFB, VEGFC and VEGFD). Raw data (Ct values) were normalized to RPL37A expression (housekeeper gene) and candidate gene expression between patient groups with differential clinical outcomes was analyzed by using Genedata Expressionist and GraphPad Prism 4 software packages. Median patient follow-up from initial diagnosis was 27 months. Results: Overexpression of VEGFA and EGFR was prominent in most tumors, but did not appear to have any prognostic value. However, VEGFC expression was significantly higher (p = 0.0002) in the tumors of patients with poor overall survival (< 27 months). Interestingly, these tumors were further characterized by significantly lower expression levels of HER2 and HER3. Median survival of patients with tumor VEGFC expression levels of >600 was calculated to be 42 months from initial diagnosis (Kaplan-Meier Survival Analysis), compared to 182 months in the rest of the patients. Conclusions: We have found that elevated VEGFC expression and low expression of HER2 and HER3 correlate with poor outcome in recurrent HNSCC patients. VEGFC preferably binds to the VEGFR3, which is predominantly expressed on lymphatic vessels. Overexpression of VEGFC may therefore result in the establishment of intratumoral lymphatic vessels, which have been shown to facilitate the dissemination of tumor cells into lymph nodes and the formation of distant metastases. We conclude that the determination of VEGFC, HER2 and HER3 expression may be of high prognostic value in HNSCC patients and that it may serve in the early identification of aggressive HNSCC subtypes. No significant financial relationships to disclose.

Secker, Genevieve A. y Natasha L. Harvey. "Regulation of VEGFR Signalling in Lymphatic Vascular Development and Disease: An Update". International Journal of Molecular Sciences 22, n.º 14 (20 de julio de 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 diseases. Lymphatic vascular development is initiated during embryogenesis following establishment of the major blood vessels and the onset of blood flow. Lymphatic endothelial progenitor cells arise from a combination of venous and non-venous sources to generate the initial lymphatic vascular structures in the vertebrate embryo, which are then further ramified and remodelled to elaborate an extensive lymphatic vascular network. Signalling mediated via vascular endothelial growth factor (VEGF) family members and vascular endothelial growth factor receptor (VEGFR) tyrosine kinases is crucial for development of both the blood and lymphatic vascular networks, though distinct components are utilised to different degrees in each vascular compartment. Although much is known about the regulation of VEGFA/VEGFR2 signalling in the blood vasculature, less is understood regarding the mechanisms by which VEGFC/VEGFD/VEGFR3 signalling is regulated during lymphatic vascular development. This review will focus on recent advances in our understanding of the cellular and molecular mechanisms regulating VEGFA-, VEGFC- and VEGFD-mediated signalling via VEGFRs which are important for driving the construction of lymphatic vessels during development and disease.

Sanmartin, 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, n.º 15_suppl (20 de mayo de 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. Differences were considered statistically significant at p<0.05. Results: We found that tumor samples had a significant higher expression of PIGF and lower expression of VEGFD, VEGFR2, and VEGFR3 compared with normal tissue (2.76X, 0.035X, 0.417X and 0.426X, respectively). The group of patients with higher expression levels of VEGFA or PlGF had a significantly reduced TTP (p=0.024 and p=0.027, respectively) and OS (p=0.055 and p=0.048, respectively) whereas those patients with values of VEGFB or VEGFD below the median had reduced TTP (p=0.020 and p=0.135, respectively) and OS (p=0.003 and p=0.089, respectively). The multivariate Cox regression analysis revealed that VEGFA, VEGFB and PlGF were independent prognostic markers for TTP and OS and based on these results we generated an “angiogenic” risk score model. TTP and OS were significantly different among the low, medium and high risk score patients (Table). Conclusions: VEGF family members are master control genes of the angiogenic process and have a crucial role in the prognostic of the disease. We found differences in the expression of four genes between tumor and normal lung samples. An “angiogenic” risk score (based on the expression of PlGF, VEGF-A and VEGF-B) significantly predicts OS and TTP in our cohort of early-stage NSCLC patients. Validation in an independent cohort is needed. Supported by grants PS09-01149 and RD06/0020/1024 from ISCIII. [Table: see text]

Jantus-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, n.º 15_suppl (20 de mayo de 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 patients were carefully micro-dissected. RNA isolated from the samples was retrotranscripted and preamplified. RTqPCR was performed using hydrolysis probes (TaqMan, Applied Biosystems) and relative quantification was calculated using GAPDH and CDKN1B as endogenous controls. Results were normalized against a human cDNA (Clontech) as a reference. All statistical analyses were considered significant at p<0.05. Results: Paired Wilcoxon test revealed differences between tumor and stroma gene expression for VEGFB (p<0.0001), VEGFC (p<0.0001), VEGFR-1 (p<0.0001), VEGFR-2 (p=0.020), VEGFR-3 (p< 0.0001), NRP-1 (p=0.001) and NRP-2 (p< 0.0001). Survival analyses showed that those patients with higher levels of the Ratio Stromal-VEGFA/ Tumoral-VEGFR-2 had worse time to progression (TTP) (median 26.23 months vs NR, p=0.013) and overall survival (OS) (median 29.50 months vs NR, p=0.001). Similarly, those patients with higher levels of the Ratio Stromal-VEGFC/Tumoral-VEGFR-3 had worse TTP (median 23.30 vs 70.53 months, p=0.015) and OS (median 37.20 months vs NR, p=0.023). Conclusions: Our results show significant differences in the expression of VEGF family members between tumor and stromal cells. This may indicate the importance of the tumor-stroma interaction when trying to understand the angiogenic process. Furthermore, the combination of the ligands expression in stroma and their receptors in tumor may have a prognostic value in NSCLC patients. Supported by grants PS09-01149 and RD06/0020/1024 from ISCIII.

Hunter, Stephanie, Braydon Nault, Kingsley Chukwunonso Ugwuagbo, Sujit Maiti y Mousumi Majumder. "Mir526b and Mir655 Promote Tumour Associated Angiogenesis and Lymphangiogenesis in Breast Cancer". Cancers 11, n.º 7 (4 de julio de 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 (ER) positive MCF7 breast cancer cells resulted in upregulation of angiogenesis and lymphangiogenesis markers vascular endothelial growth factor A (VEGFA); VEGFC; VEGFD; COX-2; lymphatic vessel endothelial hyaluronan receptor-1 (LYVE1); and receptors VEGFR1, VEGFR2, and EP4. Further, miRNA-high cell free conditioned media promoted migration and tube formation by human umbilical vein endothelial cells (HUVECs), and upregulated VEGFR1, VEGFR2, and EP4 expression, showing paracrine stimulation of miRNA in the tumor microenvironment. The miRNA-induced migration and tube formation phenotypes were abrogated with EP4 antagonist or PI3K/Akt inhibitor treatments, confirming the involvement of the EP4 and PI3K/Akt pathway. Tumour supressor gene PTEN was found to be downregulated in miRNA high cells, confirming that it is a target of both miRNAs. PTEN inhibits hypoxia-inducible factor-1 (HIF1α) and the PI3K/Akt pathway, and loss of regulation of these pathways through PTEN results in upregulation of VEGF expression. Moreover, in breast tumors, angiogenesis marker VEGFA and lymphangiogenesis marker VEGFD expression was found to be significantly higher compared with non-adjacent control, and expression of miR526b and miR655 was positively correlated with VEGFA, VEGFC, VEGFD, CD31, and LYVE1 expression in breast tumour samples. These findings further strengthen the role of miRNAs as breast cancer biomarkers and EP4 as a potential therapeutic target to abrogate miRNA-induced angiogenesis and lymphangiogenesis in breast cancer.

McCarter, Anna L. y Michael T. Dellinger. "Trametinib Inhibits Lymphatic Vessel Invasion of Bone in a Mouse Model of Gorham-Stout Disease". Journal of Vascular Anomalies 4, n.º 4 (15 de noviembre de 2023): e070. http://dx.doi.org/10.1097/jova.0000000000000070.

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Objective: Gorham-Stout disease (GSD) is a rare lymphatic anomaly that can be caused by somatic activating mutations in KRAS. This discovery has led investigators to suggest that MEK inhibitors could be a novel treatment for GSD. However, the effect of MEK inhibitors on bone disease in animal models of GSD has not been investigated. We recently reported that Osx-tTA;TetO-Vegfc mice exhibit a phenotype that resembles GSD. Osx-tTA;TetO-Vegfc mice overexpress vascular endothelial growth factor-C (VEGF-C) in bone, which stimulates the development of lymphatic vessels in bone and the gradual loss of cortical bone. The objective of this study was to characterize the effect of trametinib, an FDA-approved MEK1/2 inhibitor, on lymphangiogenesis and osteolysis in Osx-tTA;TetO-Vegfc mice. Methods: Immunoblotting was performed to assess the effect of trametinib on VEGF-C-induced phosphorylation of ERK1/2, AKT, and S6 in primary human lymphatic endothelial cells. Prevention and intervention experiments were performed to determine the effect of trametinib on lymphangiogenesis and osteolysis in Osx-tTA;TetO-Vegfc mice. Results: We found that trametinib blocked VEGF-C-induced phosphorylation of ERK1/2 in primary human lymphatic endothelial cells. We also found that trametinib prevented VEGF-C-induced lymphatic invasion of bone and cortical bone loss in Osx-tTA;TetO-Vegfc mice. Additionally, trametinib slowed the progression of disease in Osx-tTA;TetO-Vegfc mice with established disease. However, it did not reverse disease in Osx-tTA;TetO-Vegfc mice. Conclusion: Our results show trametinib impacts bone disease in Osx-tTA;TetO-Vegfc mice. These findings further support the testing of MEK inhibitors in patients with GSD and other RAS pathway-driven complex lymphatic anomalies with bone involvement.

Lim, 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, n.º 20 (27 de septiembre de 2019): 1764–75. http://dx.doi.org/10.1182/blood.2019001736.

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Key Points Platelet activation supports lymphatic vessel growth during wound healing through release of the lymphangiogenic factor VEGFC. Thrombin and plasmin support lymphatic vessel growth through proteolytic activation of the lymphangiogenic factors VEGFC and VEGFD.

Dumond, Aurore, Christopher Montemagno, Valérie Vial, Renaud Grépin y Gilles Pagès. "Anti-Vascular Endothelial Growth Factor C Antibodies Efficiently Inhibit the Growth of Experimental Clear Cell Renal Cell Carcinomas". Cells 10, n.º 5 (17 de mayo de 2021): 1222. http://dx.doi.org/10.3390/cells10051222.

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Despite improvement during the last ten years in the longevity of patients with metastatic clear cell renal cell carcinoma (mccRCC) the disease remains incurable. Hence, new therapeutic strategies are urgently needed. Relapse following anti-angiogenic treatment depends on the over-expression of vascular endothelial growth factor C (VEGFC), one of the main drivers of lymphangiogenesis. Therefore, we developed specific mouse monoclonal antibodies and evaluated their therapeutic efficacy in vitro and in vivo. Immunization of mice with the domain of VEGFC that stimulates the VEGF receptor 3 (VEGFR3) led to the selection of one hybridoma producing specific anti-VEGFC monoclonal antibodies. The selected 1E9 antibodies were sequenced, and the corresponding variable light and heavy chains were subcloned into expression vectors in frame with sequences encoding the human IgG1 constant heavy and light chains. CHO cells were stably transfected and cloned to produce chimeric antibodies. These antibodies inhibited the activation of VEGFR3 signaling, and therefore the proliferation and migration of VEGFC-stimulated endothelial cells. Moreover, they inhibited the proliferation of VEGFC-expressing renal cancer cells through NRP2 signaling. 1E9 antibodies inhibited the growth of experimental RCC, and their therapeutic efficacy was enhanced by the anti-VEGF antibody bevacizumab. Hence, our results suggest that targeting VEGFC could have a relevant therapeutic impact on mccRCC that relapse following anti-angiogenic treatment.

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Tesis sobre el tema "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 patients au diagnostic ou après une rechute.Les MB sont des tumeurs très vascularisées. Le phénomène de résistance est, en partie, lié au développement de vaisseaux sanguins (angiogenèse) et lymphatiques (lymphangiogenèse) dans la tumeur, qui constituent les principales voies de dissémination métastatique. Le facteur de croissance des vaisseaux lymphatiques, le VEGFC, et ses récepteurs/co-récepteurs sont les acteurs majeurs de la lymphangiogenèse. Dans la première partie de ma thèse, j'ai montré que le VEGFC est inversement corrélé à la croissance et l'agressivité cellulaire du MB. En effet, le VEGFC diminue de manière autocrine la prolifération et la migration des cellules MB, ainsi que leur capacité à former des pseudo-vaisseaux in vitro. Les cellules résistantes à la radiothérapie présentent des niveaux élevés de VEGFC et perdent leur capacité à migrer et à former des pseudo-vaisseaux. L'irradiation réduit l'agressivité des cellules de MB par un processus dépendant du VEGFC. Les cellules surexprimant le VEGFC et les cellules résistantes à l'irradiation forment des tumeurs expérimentales plus petites chez la souris Nude. Le VEGC semble être un régulateur négatif de la croissance des MB. Ces résultats ouvrent la voie au développement de thérapies pro-VEGFC dans ces cancers.Dans la seconde partie de ma thèse, j'ai corrélé l'expression de la voie de signalisation pro-angiogénique et pro-inflammatoire ELR+CXCL/CXCR1-2 à une survie plus courte chez des patients atteints de MB. J'ai montré qu'un nouvel inhibiteur pharmacologique (C29) des récepteurs CXCR1-2 inhibe la prolifération, la migration dépendante de CXCL8/CXCR1/2, l'invasion et la formation de pseudo-vaisseaux par des cellules de MB sensibles ou résistantes à la radiothérapie. C29 réduit la croissance de MB expérimentaux dans un modèle de souris organotypique ex vivo et traverse la barrière hémato-encéphalique. Ainsi, le ciblage de CXCR1-2 représente une stratégie prometteuse pour le traitement des MB pédiatriques, en première ligne ou à la suite de rechutes.Mots-clés : médulloblastome pédiatrique, VEGFC/VEGFR, CXCR1-2, cytokines ELR+CXCL, thérapie ciblée, lymphangiogenèse, angiogenèse
Medulloblastoma (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.

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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-aortic lymph node infiltration by HOCS neoplastic cells. Histological detection of tumor cells in blood and lymphatic vessels indicated both hematogenous and lymphatic dissemination. VEGFC was over-expressed in the VEGFR3-positive and luciferase-expressing lA9 and IGROVl ovarian cancer cells. In vitro. VEGFC released by the expressing turnor cells stimulated turnor cell migration in an autocrine manner. In vivo, over-expression of VEGFC promoted . IGROVl dissemination after orthotopic intraovarian transplantation in nude mice. VEGFC released in serum of mice correlated with tumor burden and metastasis. Cediranib, a small molecule receptor tyrosine kinase inhibitor of VEGFRl-3 and c-Kit, inhibited in vivo metastasis of VEGFC-overexpressing [GROVI and in vitro autocrine effects on turnor cell migration; cediranib improved the survival of mice bearing the four HOC xenografts analyzed. The therapeutic benefit was proportional to soluble VEGFC levels in serum and ascites and to VEGFR3 expression by tumor cells. Different schedules of cediranib were tested on HOC8 xenograft, The survival benefit of cediranib in maintenance regimen (14 weeks) was superior to 3-weeks treatment. A significant prolongation of mice survival was observed in mice treated with advanced turnor. Treatment benefits were improved combining cediranib with chemotherapy (paclitaxel plus cisplatin). These findings suggest that the VEGFCNEGFR3 pathway acts as an enhancer of ovarian cancer progression through autocrine and paracrine mechanisms, hence offering a potential target for therapy.

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) foram avaliadas por imunohistoquímica, seguidas de estereologia, após a cirurgia com ou sem o tratamento com VEGFC exógeno. O grupo controle não foi manipulado, mas recebeu soro fisiológico em vez de tratamento com VEGFC exógeno. As expressões do VEGFC e FLT4 local foram avaliadas por qPCR. Houve efeito do tempo sobre Vv e Lv no Grupo Cirurgia e diferença significativa entre os grupos Controle e Cirurgia nas três regiões estudadas (região proximal, média e distal) do MP esquerdo (MPE). A Lv mostrou diferença significativa entre os grupos Controle e Cirurgia somente na região média do MPE. A Vv e a Lv para o Grupo Tratamento foram maiores do que os outros grupos em todas as regiões do MPE. A expressão gênica do VEGFC e do FLT4 apresentou efeito do tempo em todas as regiões do MPE para os grupos Cirurgia e Tratamento. Ambas as expressões gênicas do VEGFC e do FLT4 apresentaram diferença significativa entre os grupos Controle e Cirurgia, entre os grupos Cirurgia e Tratamento e entre os grupos Controle e Tratamento. Os resultados mostraram que os camundongos são bons modelos experimentais para o uso de VEGFC exógeno como terapia de revascularização linfática, e o tratamento com VEGFC exógeno aumenta vascularização linfática já após 3 dias de dano linfático.
Lymphatic 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.

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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 lymphatic vasculature, I characterized this process in Ang2-/- mice. Indeed, lymphatic vessels in the skin of Ang2-/- pups prematurely recruited SMCs and did not mature into collecting vessels during the remodeling stage of lymphatic development. In contrast, Ang2 knockout Ang1 knock-in mice did develop a hierarchal lymphatic vasculature, suggesting that activation of Tie-2 is required for normal lymphatic development. To further delineate the molecular mechanisms regulating lymphatic development, I also characterized Chylous ascites-3 (Chy-3) mice, a strain missing cytobands 8A4 to 8B3 from one copy of chromosome 8. Real-time PCR using genomic DNA demonstrated that the lymphangiogenesis gene, Vegfc, was included in the deleted region. All of the key components of a normal lymphatic network had developed in Chy-3 mice; however, the number of lymphatic vessels was reduced. Although the patterning of lymphatic vasculature in Chy-3 mice was altered, the architecture of the blood vasculature appeared normal. Ang2-/- and Chy-3 mice are grossly indistinguishable from one another; however, their underlying lymphatic defects are dramatically different. Ang2-/- mice exhibit defects in lymphangiogenic remodeling and lymphangiogenesis, whereas Chy-3 mice show a reduced capacity for lymphangiogenesis. I propose that Ang2 maintains lymphatic vessel plasticity by preventing SMC-lymphatic vessel associations so maturation can occur and facilitates lymphangiogenesis in the presence of Vegfc. This is analogous to Ang2's function on the blood vasculature where it is thought to destabilize SMC-blood vessel interactions and facilitate hemangiogenesis in the presence of Vegfa.Taken together, these findings further delineate the development of the lymphatic system and could provide translational clues relevant to the pathogenesis and treatment of clinical disorders of the lymphatic system.

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 expressos pelo epitélio luminal e glandular e fracamente pelo estroma endometrial. Do 5º ao 8º dias de gestação, o VEGF foi expresso nas células deciduais mesometriais. VEGFR1 e VEGFR2 foram expresso pelas células do epitélio luminal e glandular e mostraram uma marcação diferencial na decídua mesometrial e antimesometrial. Os receptores VEGFR1 e VEGFR2 foram intensamente expressos pelas células endoteliais dos capilares sinusóides mesometriais e pelas células Nk uterinas.
In 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.

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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 seconde approche reposant sur la conception de peptides ciblant le VEGF a alors été initiée. A partir d’un peptide cyclique connu de 19 résidus ayant une affinité submicromolaire pour le VEGF, de nouveaux peptides et peptidomimétiques ont été développés.L’objectif a été de concevoir des composés de structures chimiques potentiellement plus simples et plus stables en milieu biologique, tout en optimisant l’affinité pour le VEGF. L’interaction de ces peptides avec le VEGF a été étudiée in vitro par ELISA et ITC, ainsi que par cristallographie pour le composé le plus affin. En parallèle, nous avons étudié l’effet du cuivre et d’autres métaux divalents sur l’interaction VEGF/VEGFR1. Au travers d’expériences réalisées au laboratoire ainsi qu’en collaboration, nous avons montré que certains métaux étaient capables non seulement d’inhiber l’interaction VEGF/VEGFR1 mais également d’induire une dimérisation non classique du domaine 2du récepteur. Sachant que les métaux, et en particulier le cuivre, sont connus pour jouer un rôle important dans l’angiogenèse, cette découverte apporte de nouveaux éléments de réponse sur leur mécanisme d’action. Ce travail de thèse s’inscrit donc non seulement dans une démarche de développement de nouveaux composés anti-angiogéniques mais également de compréhension du mécanisme de régulation de l’angiogenèse
Inhibiting 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/.

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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 optique chez la souris. J’ai localisé par hybridation in situ les sites d’expression du Vegf-c et du Vegfr-3 dans les régions septo-hippocampale, pré-thalamique et dorso-latérale du thalamus du cerveau embryonnaire et adulte de poulet. En effet, le modèle de poulet est très utilisé pour ce genre de manipulation du fait de son accessibilité aux stades embryonnaires. J’ai ensuite généré et testé la validité d’une série d’outils moléculaires permettant de bloquer par ARN interférence l’expression du Vegfr-3 (siRNAs et shRNAs codé par un plasmide pouvant être électroporé ou dans un lentivirus capable d’infecter durablement le cerveau embryonnaire et adulte). J’ai mis au point la technique d’électroporation et permis d’engager les expériences d’ARN interférence actuellement en cours. J’ai également mis au point les analyses fonctionnelles permettant d’évaluer les effets de la perte de fonction du VEGFR-3 sur la prolifération, la survie, la mise en place des populations neuronales exprimant le gène codant le Vegfr-3 dans le septum et ainsi que sur le développement des projections axonales connectant l’hippocampe dans lequel le Vegf-c est exprimé.

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Libros sobre el tema "Vegfc":

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

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

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

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

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

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

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

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

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Duker, Jay y Michelle Liang. Anti-VEGF Use in Ophthalmology. Boca Raton: 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. Birmingham: University of Birmingham, 1999.

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Capítulos de libros sobre el tema "Vegfc":

Farooqi, Ammad Ahmad y Ilhan Yaylim. "miRNA Regulation of VEGF/VEGFR Signaling". En MicroRNA Targeted Cancer Therapy, 309–25. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05134-5_17.

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Escudier, Bernard y Laurence Albiges. "Anti-VEGF and VEGFR Monoclonal Antibodies in RCC". En Renal Cell Carcinoma, 237–52. New York, NY: 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 y Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings". En 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.

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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 inhibition, novel therapies under evaluation are directed against vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR), PI3K/AKT/mTOR pathway, cell cycle regulation (for example, cyclin dependent kinases 4 and 6), HRAS, DNA repair mechanisms, and others. Development of new therapies has to take into consideration the complexity of solid tumors and their heterogeneity. Multitargeted combination therapy approaches may be required in certain cases in order to maximize antitumor effect. Ways to individualize treatment using validated biomarkers are likely to improve outcomes. We review the most relevant molecular targets in HNSCC and provide updates on clinical trial data with promising new targeted agents.

de Groot, Heink, Vera Schmit-Eilenberger, Janna Kirchhof y Albert J. Augustin. "Angiostatic and Angiogenic Factors". En Anti-VEGF, 1–3. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320005.

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Siemerink, Martin J., Albert J. Augustin y Reinier O. Schlingemann. "Mechanisms of Ocular Angiogenesis and Its Molecular Mediators". En Anti-VEGF, 4–20. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320006.

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Schmidt-Erfurth, Ursula, Andreas Pollreisz, Christoph Mitsch y Matthias Bolz. "Antivascular Endothelial Growth Factors in Age-Related Macular Degeneration". En Anti-VEGF, 21–38. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320007.

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Iacono, Pierluigi, Maurizio Battaglia Parodi y Francesco Bandello. "Antivascular Endothelial Growth Factor in Diabetic Retinopathy". En Anti-VEGF, 39–53. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320008.

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Buehl, Wolf, Stefan Sacu y Ursula Schmidt-Erfurth. "Retinal Vein Occlusions". En Anti-VEGF, 54–72. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320009.

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Battaglia Parodi, Maurizio, Pierluigi Iacono y Francesco Bandello. "Antivascular Endothelial Growth Factor for Choroidal Neovascularization in Pathologic Myopia". En Anti-VEGF, 73–83. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320010.

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Battaglia Parodi, Maurizio, Pierluigi Iacono, Frank D. Verbraak y Francesco Bandello. "Antivascular Endothelial Growth Factors for Inflammatory Chorioretinal Disorders". En Anti-VEGF, 84–95. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320011.

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Actas de conferencias sobre el tema "Vegfc":

Odarenko, K. V., O. V. Salomatina, N. F. Salakhutdinov, M. A. Zenkova y A. V. Markov. "SEARCH FOR REGULATORY GENES AND SMALL-MOLECULAR INHIBITORS OF THE HIGHLY AGGRESSIVE PHENOTYPE OF GLIOBLASTOMA". En 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.

"VEGFC and INHBA as new molecular markers of the glial-mesenchymal transition". En 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, Jean-Christophe Thery, Stephane Vignot, Morgan Roupret, Jean-Philippe Spano y David Khayat. "Abstract 5138: Expression and circulating levels of VEGFC/VEGFD and their receptor VEGFR2, R3 in renal cell cancer: Relationship with clinicopathological parameters". En 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 y Rajvir Dahiya. "Abstract 2293: MicroRNA-1826 targets VEGFC, beta-catenin (CTNNB1) and MEK1 (MAP2K1) in human bladder cancer." En 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 y Shi-Qian Zhang. "VEGF-C, VEGF-D, and VEGFR-3 and their roles in lymphatic metastasis of tumors". En 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 y Samia Mourah. "Abstract 5284: EMMPRIN mediates VEGF activation of VEGFR-2 in melanoma cells". En 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, Pierre Triozzi, Afshin Dowlati, Ernest Borden y Brian Rini. "Abstract 1184: The effect of dual VEGF/VEGFR inhibition on angiogenic signaling pathways." En 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 y Nygel Wynn. "Abstract 5157: A role of the FGF-pathway in the VEGF/VEGFR targeting". En 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 y Norbert F. Voelkel. "Inhibition Of VEGFr-2 Induces Apoptosis And VEGF Protein Expression In Human Pulmonary Microvascular Endothelial Cells". En 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 y Kevin C. Gatter. "Abstract B25: Autocrine action of VEGF/VEGFR pathway in human Glioblastomas in addition to the paracrine angiogenic role". En 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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Informes sobre el tema "Vegfc":

Chen, Cheng-Che y 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, marzo de 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 the PFS and OS of anti-VEGF agents vs. IFN-alpha for patients with RCC. Part 4. The relative risk (RR) of bleeding events of anti-VEGF agents vs. placebo or IFN-alpha for patients with RCC.

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

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

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

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Bobykin, Evgenij, Sergej Korotkih, Ol'ga Morozova y Vadim Krohalev. Anti-VEGF Therapy for Macular Diseases: From Theory to Practice (Interactive Electronic Training Manual). SIB-Expertise, diciembre de 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 описаниями клинических примеров лечения пациентов с неоваскулярной возрастной макулярной дегенерацией, диабетическим макулярным отёком, отёком макулы вследствие окклюзии ретинальных вен и миопической хориоидальной неоваскуляризацией. Пособие может быть полезным для самостоятельного овладения офтальмологом знаниями и навыками применения антиангиогенной терапии в практической работе. Читательское назначение: для врачей-офтальмологов, слушателей курсов дополнительного профессионального образования и непрерывного медицинского образования. Интерактивное электронное учебно-методическое пособие может быть использовано в качестве дополнительной литературы в процессе освоения образовательных программ высшего образования, ординатуры и аспирантуры по специальности «Офтальмология». 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 описаниями клинических примеров лечения пациентов с неоваскулярной возрастной макулярной дегенерацией, диабетическим макулярным отёком, отёком макулы вследствие окклюзии ретинальных вен и миопической хориоидальной неоваскуляризацией. Пособие может быть полезным для самостоятельного овладения офтальмологом знаниями и навыками применения антиангиогенной терапии в практической работе. Читательское назначение: для врачей-офтальмологов, слушателей курсов дополнительного профессионального образования и непрерывного медицинского образования. Интерактивное электронное учебно-методическое пособие может быть использовано в качестве дополнительной литературы в процессе освоения образовательных программ высшего образования, ординатуры и аспирантуры по специальности «Офтальмология».

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

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

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

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Gabhann, Feilim M. Computational Models of Anti-VEGF Therapies in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, junio de 2013. http://dx.doi.org/10.21236/ada582842.

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Contreras, Muricio A. Lymphatic Regeneration within Porous VEGF-C Hydrogels for Secondary Lymphedema. Fort Belvoir, VA: Defense Technical Information Center, julio de 2002. http://dx.doi.org/10.21236/ada410086.

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