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Добірка наукової літератури з теми "VEGFRs"

Автор: Grafiati

Опубліковано: 10 березня 2023

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Статті в журналах з теми "VEGFRs"

Bais, Swarna, Elizabeth Wise, Eric M. Harris, Amy Meacham, and Christopher R. Cogle. "AML Depends on VEGFR1 and Not VEGFR2 for Proliferation and Protection From Chemotherapy,." Blood 118, no. 21 (November 18, 2011): 3598. http://dx.doi.org/10.1182/blood.v118.21.3598.3598.

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Abstract Abstract 3598 Background: Vascular endothelial growth factor (VEGF) and its cognate receptors (VEGFRs) are known to serve important roles in normal hematopoiesis, but the importance of the VEGF/VEGFR axis in malignant hematopoiesis, namely acute myeloid leukemia (AML), is poorly defined. Methods: Bone marrow from AML patients were analyzed for VEGFRs on the malignant myeloblast populations. Human myeloid leukemia cell lines, KG-1, HL60 and K562, were also evaluated for VEGFR expression. Knockdown of VEGFR1 and VEGFR2 receptors in AML cells expressing these receptors were performed using lentivirus transfection of shRNA. Cell proliferation was quantified using XTT colorimetric assay and apoptosis was evaluated by Annexin V and PI staining. Results: Bone marrow from 12 consecutive AML patients showed that 33% of patients had malignant myeloblasts that expressed VEGFR1. Of the AML cell lines tested, only KG-1 cells expressed VEGFR1 and VEGFR2. Knockdown of VEGFR1 and VEGFR2 in KG-1 cells were confirmed by Western blot. When VEGFR1 was knocked down in KG-1 leukemia cells, cell proliferation was significant decreased (Figure 1). In addition, knocking down VEGFR1 resulted in enhanced sensitivity to cytarabine chemotherapy (Figure 1). In contrast, knockdown of VEGFR2 did not result in changes in leukemia cell proliferation or sensitivity to cytarabine chemotherapy (Figure 2). When KG-1 leukemia cells knocked down for VEGFR1 expression were transplanted into sublethally, irradiated NOD/scid/IL2R□−/− (NSG) mice (n=10), none of the mice showed engraftment of VEFR1 deficient cells. Conclusions: The VEGF/VEGFR axis is an important determinant in AML pathobiology. In specific, AML cells depend upon VEGFR1 and this receptor represents a promising target for future therapeutic intervention. Disclosures: No relevant conflicts of interest to declare.

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Zarkada, Georgia, Krista Heinolainen, Taija Makinen, Yoshiaki Kubota, and Kari Alitalo. "VEGFR3 does not sustain retinal angiogenesis without VEGFR2." Proceedings of the National Academy of Sciences 112, no. 3 (January 5, 2015): 761–66. http://dx.doi.org/10.1073/pnas.1423278112.

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Angiogenesis, the formation of new blood vessels, is regulated by vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs). VEGFR2 is abundant in the tip cells of angiogenic sprouts, where VEGF/VEGFR2 functions upstream of the delta-like ligand 4 (DLL4)/Notch signal transduction pathway. VEGFR3 is expressed in all endothelia and is indispensable for angiogenesis during early embryonic development. In adults, VEGFR3 is expressed in angiogenic blood vessels and some fenestrated endothelia. VEGFR3 is abundant in endothelial tip cells, where it activates Notch signaling, facilitating the conversion of tip cells to stalk cells during the stabilization of vascular branches. Subsequently, Notch activation suppresses VEGFR3 expression in a negative feedback loop. Here we used conditional deletions and a Notch pathway inhibitor to investigate the cross-talk between VEGFR2, VEGFR3, and Notch in vivo. We show that postnatal angiogenesis requires VEGFR2 signaling also in the absence of Notch or VEGFR3, and that even small amounts of VEGFR2 are able to sustain angiogenesis to some extent. We found that VEGFR2 is required independently of VEGFR3 for endothelial DLL4 up-regulation and angiogenic sprouting, and for VEGFR3 functions in angiogenesis. In contrast, VEGFR2 deletion had no effect, whereas VEGFR3 was essential for postnatal lymphangiogenesis, and even for lymphatic vessel maintenance in adult skin. Knowledge of these interactions and the signaling functions of VEGFRs in blood vessels and lymphatic vessels is essential for the therapeutic manipulation of the vascular system, especially when considering multitargeted antiangiogenic treatments.

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Witmer, Antonella N., Jiapei Dai, Herbert A. Weich, Gijs F. J. M. Vrensen, and Reinier O. Schlingemann. "Expression of Vascular Endothelial Growth Factor Receptors 1, 2, and 3 in Quiescent Endothelia." Journal of Histochemistry & Cytochemistry 50, no. 6 (June 2002): 767–77. http://dx.doi.org/10.1177/002215540205000603.

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The vascular endothelial growth factor (VEGF) family is involved in angiogenesis, and therefore VEGFs are considered as targets for anti-angiogenic therapeutic strategies against cancer. However, the physiological functions of VEGFs in quiescent tissues are unclear and may interfere with such systemic therapies. In pathological conditions, increased levels of expression of the VEGF receptors VEGFR-1, VEGFR-2, and VEGFR-3 accompany VEGF activity. In this study we investigated normal human and monkey tissues for expression patterns of these receptors. Immunohistochemical staining methods at the light and electron microscopic level were applied to normal human and monkey tissue samples, using monoclonal antibodies (MAbs) against the three VEGFRs and anti-endothelial MAbs PAL-E and anti-CD31 to identify blood and lymph vessels. In human and monkey, similar distribution patterns of the three VEGFRs were found. Co-expression of VEGFR-1, −2, and −3 was observed in microvessels adjacent to epithelia in the eye, gastrointestinal mucosa, liver, kidney, and hair follicles, which is in line with the reported preferential expression of VEGF-A in some of these epithelia. VEGFR-1, −2, and −3 expression was also observed in blood vessels and sinusoids of lymphoid tissues. Furthermore, VEGFR-1, but not VEGFR-2 and −3, was present in microvessels in brain and retina. Electron microscopy showed that VEGFR-1 expression was restricted to pericytes and VEGFR-2 to endothelial cells in normal vasculature of tonsils. These findings indicate that VEGFRs have specific distribution patterns in normal tissues, suggesting physiological functions of VEGFs that may be disturbed by systemic anti-VEGF therapy. One of these functions may be involvement of VEGF in paracrine relations between epithelia and adjacent capillaries.

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Morimoto, Yukina, Masahiro Toda, Ryota Tamura, Kentarou Ohara, Yumiko Oishi, and Kazunari Yoshida. "IMT-02 VEGF RECEPTORS EXPRESSION AND REPORT OF CLINICAL TRIAL OF PEPTIDE VACCINE IN SKULL BASE CHORDOMA." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii17. http://dx.doi.org/10.1093/noajnl/vdz039.077.

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Abstract Chordoma is a rare refractory neoplasm that arises from the embryological remnants of the notochord. Vascular endothelial growth factor (VEGF) is a potent activator of angiogenesis that is associated with the tumor-immune microenvironment. To evaluate the characteristics of vascular and tumor cells in chordoma, we first analyzed the expression of VEGF receptor (VEGFR) 1, VEGFR2, CD34, and Brachyury in a cell line and 54 tumor tissues. Patients with primary skull base chordomas were divided into the two groups as per the tumor growth rate. The expressions of VEGF-A, VEGFR1, and VEGFR2 on tumor cells; tumor infiltrative immune cells, including regulatory T cells (Tregs) and tumor-associated macrophages (TAMs); and immune-checkpoint molecules (PD-1/PD-L1) were analyzed with the clinical courses. Both VEGFR1 and VEGFR2 were strongly expressed not only on vascular endothelial cells, but also on tumor cells. The recurrent cases showed significantly higher VEGFR1 expressions on tumor cells than the primary cases. The expression of VEGF-A, and the numbers of CD163+ TAMs and Foxp3+ Tregs were significantly higher in the patients with rapid progressive course than the patients with slow progressive course. Based on the present results, VEGFRs-targeted therapy may show efficacy in regulating growth of chordomas.

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Feng, Yan, Ying Li, Xinling Yang, Limin Han, Luning Wang, Shan Gao, Ruixue Yin, et al. "Direct evidence of VEGF-mediated neuroregulation and afferent explanation of blood pressure dysregulation during angiogenic therapy." Frigid Zone Medicine 1, no. 2 (December 1, 2021): 119–26. http://dx.doi.org/10.2478/fzm-2021-0015.

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Abstract Objective Oncocardiology is increasingly hot research field/topic in the clinical management of cancer with anti-angiogenic therapy of vascular endothelial growth factor (VEGF) that may cause cardiovascular toxicity, such as hypertension via vascular dysfunction and attenuation of eNOS/NO signaling in the baroreflex afferent pathway. The aim of the current study was to evaluate the potential roles of VEGF/VEGF receptors (VEGFRs) expressed in the baroreflex afferent pathway in autonomic control of blood pressure (BP) regulation. Methods The distribution and expression of VEGF/VEGFRs were detected in the nodose ganglia (NG) and nucleus of tractus solitary (NTS) using immunostaining and molecular approaches. The direct role of VEGF was tested by NG microinjection under physiological and hypertensive conditions. Results Immunostaining data showed that either VEGF or VEGFR2/VEGFR3 was clearly detected in the NG and NTS of adult male rats. Microinjection of VEGF directly into the NG reduced the mean blood pressure (MBP) dose-dependently, which was less dramatic in renovascular hypertension (RVH) rats, suggesting the VEGF-mediated depressor response by direct activation of the 1st-order baroreceptor neurons in the NG under both normal and disease conditions. Notably, this reduced depressor response in RVH rats was directly caused by the downregulation of VEGFR2, which compensated the up regulation of VEGF/VEGFR3 in the NG during the development of hypertension. Conclusion It demonstrated for the first time that the BP-lowering property of VEGF/VEGFRs signaling via the activation of baroreflex afferent function may be a common target/pathway leading to BP dysregulation in anti-angiogenic therapy.

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Coon, Brian G., Nicolas Baeyens, Jinah Han, Madhusudhan Budatha, Tyler D. Ross, Jennifer S. Fang, Sanguk Yun, Jeon-Leon Thomas, and Martin A. Schwartz. "Intramembrane binding of VE-cadherin to VEGFR2 and VEGFR3 assembles the endothelial mechanosensory complex." Journal of Cell Biology 208, no. 7 (March 23, 2015): 975–86. http://dx.doi.org/10.1083/jcb.201408103.

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Endothelial responses to fluid shear stress are essential for vascular development and physiology, and determine the formation of atherosclerotic plaques at regions of disturbed flow. Previous work identified VE-cadherin as an essential component, along with PECAM-1 and VEGFR2, of a complex that mediates flow signaling. However, VE-cadherin’s precise role is poorly understood. We now show that the transmembrane domain of VE-cadherin mediates an essential adapter function by binding directly to the transmembrane domain of VEGFR2, as well as VEGFR3, which we now identify as another component of the junctional mechanosensory complex. VEGFR2 and VEGFR3 signal redundantly downstream of VE-cadherin. Furthermore, VEGFR3 expression is observed in the aortic endothelium, where it contributes to flow responses in vivo. In summary, this study identifies a novel adapter function for VE-cadherin mediated by transmembrane domain association with VEGFRs.

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Dewaele, B., G. Floris, R. Sciot, H. Prenen, A. Wozniak, L. Guillou, J. Coindre, C. Fletcher, P. Schöffski, and M. Debiec-Rychter. "Tyrosine kinases as possible therapeutic targets in pulmonary artery intimal sarcoma." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 10055. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.10055.

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10055 Background: Pulmonary artery intimal sarcomas (PAIS) are very rare, highly malignant and clinically aggressive tumors, with yet elusive underlying pathogenic mechanisms and histogenesis. Our aim was to gain molecular insight in the oncogenic events leading to PAIS development, and to investigate the possibility of a pharmacological approach for the treatment of PAIS, specifically targeting the receptor tyrosine kinases (RTK) activated in these tumors. Methods: Fourteen cases of advanced high grade poorly differentiated PAIS were analyzed by immunohistochemistry and selectively by a variety of cytogenetic/molecular techniques, e.g. karyotyping, FISH, mRNA in situ hybridization, array-CGH, tyrosine kinases RT-PCR assay and Western blotting analysis. The study was supplemented by sequencing of PDGFRA, PDGFRB, KIT, VEGFR-1, VEGFR-2 and EGFR genes. Ex vivo functional assays were applied to test the sensitivity of PAIS primary tumor cells to different, clinically approved RTK inhibitors. Results: We demonstrate that (1) PAIS do not have mutations within the kinase domains of PDGFRs, KIT, VEGFRs or EGFR, (2) all cases show a similar cytogenetic molecular profile, characterized by amplification of PDGFRA/KIT/VEGFR2 and MDM2/CDK4 genes, while EGFR, PDGFRB and VEGFR1 are frequently polysomic but rarely highly amplified, (3) high level of expression of PDGFRA, VEGFR1/VEGFR2 and EGFR is uniformly present in the tested tumors, (4) PAIS demonstrate activation (phosphorylation) of PDGFRA and downstream PI3K-AKT and MAP-Kinase signaling pathways, (4) in ex vivo assays, a potent effect of BMS354825 on proliferation and survival of primary cells of PAIS is proven. Conclusions: PDGFRA is amplified and activated in PAIS, thus constituting one of many possible targets for the therapy. Tested inhibitors showed differential efficacy for inhibition of PAIS cells by ex vivo assays. No significant financial relationships to disclose.

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Tamura, Ryota, Yukina Morimoto, Mizuto Sato, Tetsuro Hikichi, Kazunari Yoshida, and Masahiro Toda. "A Pilot Study of the Adverse Events Caused by the Combined Use of Bevacizumab and Vascular Endothelial Growth Factor Receptor-Targeted Vaccination for Patients with a Malignant Glioma." Vaccines 8, no. 3 (September 2, 2020): 498. http://dx.doi.org/10.3390/vaccines8030498.

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Anti-angiogenic therapy, targeting vascular endothelial growth factor (VEGF)-A/VEGF receptors (VEGFRs), is beneficial for tumor growth prevention in a malignant glioma. A simultaneous blockade using both bevacizumab (Bev), which targets circulating VEGF-A, and a multi-kinase inhibitor on VEGFRs was more effective for advanced solid cancers, including melanoma and renal cell carcinoma. However, previous clinical trials demonstrated a high adverse event rate. Additionally, no studies previously assessed treatment efficacy and safety using both VEGF-A and VEGFR-targeted agents for malignant gliomas. We had conducted clinical trials investigating VEGFRs peptide vaccination in patients with malignant gliomas, in which the treatment exhibited safety and yielded therapeutic effects in some patients. The combined use of Bev and VEGFRs vaccination may enhance the anti-tumor effect in malignant gliomas. In this pilot study, the adverse event profile in patients treated with Bev after the vaccination was investigated to establish this treatment strategy, in comparison to those treated with Bev collected from the published data or treated with the vaccination alone. In our previous clinical studies on patients with malignant gliomas, Bev was administered to 13 patients after VEGFRs vaccinations. One patient had a Grade 4 pulmonary embolism. Two patients had Grade 2 cerebral infarctions. There were no significant differences in the adverse event rates among patients treated with Bev, with the vaccination, or with Bev after the vaccination. Although careful observation is imperative for patients after this combination treatment strategy, VEGFRs-targeted vaccination may coexist with Bev for malignant gliomas.

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Zhang, Huanxiang, Laszlo Vutskits, Michael S. Pepper, and Jozsef Z. Kiss. "VEGF is a chemoattractant for FGF-2–stimulated neural progenitors." Journal of Cell Biology 163, no. 6 (December 22, 2003): 1375–84. http://dx.doi.org/10.1083/jcb.200308040.

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Mmigration of undifferentiated neural progenitors is critical for the development and repair of the nervous system. However, the mechanisms and factors that regulate migration are not well understood. Here, we show that vascular endothelial growth factor (VEGF)-A, a major angiogenic factor, guides the directed migration of neural progenitors that do not display antigenic markers for neuron- or glia-restricted precursor cells. We demonstrate that progenitor cells express both VEGF receptor (VEGFR) 1 and VEGFR2, but signaling through VEGFR2 specifically mediates the chemotactic effect of VEGF. The expression of VEGFRs and the chemotaxis of progenitors in response to VEGF require the presence of fibroblast growth factor 2. These results demonstrate that VEGF is an attractive guidance cue for the migration of undifferentiated neural progenitors and offer a mechanistic link between neurogenesis and angiogenesis in the nervous system.

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Furuya, Mitsuko, Kentaro Kurasawa, Kiyotaka Nagahama, Kae Kawachi, Akinori Nozawa, Tsuneo Takahashi, and Ichiro Aoki. "Disrupted Balance of Angiogenic and Antiangiogenic Signalings in Preeclampsia." Journal of Pregnancy 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/123717.

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The placenta plays a central role in governing local circulatory system that mediates maternal condition and fetal growth. In early gestational phases, the placenta exerts properties of invasion and neovascularization for successful placentation. Extravillous invasive trophoblasts replace uterine endometrial vasculature and establish local blood pathway to obtain oxygen and nutrients from the mother. In later phases, the placenta promotes villous angiogenesis and vascular maturation that are finely controlled by angiogenic and antiangiogenic molecules. Among various molecules involved in placental neovascularization, vascular endothelial growth factor receptors (VEGFRs) and angiotensin II receptor type 1 (AT1) mediate important signaling pathways for maternal circulatory system and fetal growth. VEGFR1 and VEGFR2 are functional receptors for placental growth factor (PlGF) and VEGF, respectively, and PlGF-VEGFR1 and VEGF-VEGFR2 interactions are disturbed in many preeclamptic patients by excess amount of soluble form of VEGFR1 (also named sFlt1), a natural PlGF/VEGF antagonist. Recent studies have disclosed that excessive sFlt1 production in the placenta and aberrant AT1 signaling in the mother are closely associated with the pathology of preeclampsia and intrauterine growth restriction (IUGR). In this paper, neovascularization of the placenta and pathological events associated with disrupted balance between angiogenic and antiangiogenic signaling in preeclampsia are discussed.

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Більше джерел

Дисертації з теми "VEGFRs"

Li, Xiaobo. "PHYSICAL INTERACTIONS BETWEEN NEUROPILIN AND VEGFRS, INTEGRINS IN REGULATING ENDOTHELIAL CELL FUNCTIONS." UKnowledge, 2015. http://uknowledge.uky.edu/biochem_etds/23.

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The neuropilin (Nrp) family consists of multifunctional cell surface receptors with critical roles in a number of different cell and tissue types. A core aspect of Nrp function is ligand-dependent cellular adhesion and migration, where it controls the multistep process of cellular motility through integration of ligand binding, receptor coupling and signaling via the coordinated action of its extracellular and intracellular domains. While Nrp regulates cellular adhesion and motility in the cardiovascular and nervous systems under physiological conditions, the emerging pathological role of Nrp in tumor cell migration and metastasis has been identified and provides motivation for continued efforts toward developing Nrp inhibitors. At the molecular level, the role of Nrp in adhesion and migration is intimately connected to the control of adhesive interactions and cytoskeletal reorganization. The adhesive “interactome” for Nrp draws much attention because of its lack of enzymatic activity and inability to transduce signals on its own. It is an active area of research and is still expanding dramatically. Nrp has been well defined as a co-receptor for vascular endothelial growth factor receptor (VEGFR)/vascular endothelial growth factor (VEGF) signaling through enhancing receptor-ligand interaction in angiogenesis. Here, we contribute to this concept through characterization in more biochemical detail about Nrp-1/VEGF physical interactions. VEGF has been shown to compete with Sema3 for binding to Nrp-1 b1 ligand binding pocket. This competition fine-tunes VEGF-induced angiogenesis. Our data provides a molecular mechanism for high affinity Sema3F binding to Nrp-1 in the b1 domain. As to the VEGFR-independent function, Nrp/integrin association has been demonstrated. The functional integration has been shown for Nrp/integrin in angiogenic sprouting. Both proteins are highly expressed in endothelial tip cells to mediate endothelial cell migration during angiogenesis and knockdown of either one in mice leads to embryonic lethality due to similar defects in vascular development. To identify the structure and function correlation, we characterized in more detail about Nrp-1/integrin physical interactions with biochemical and cell-based assays. Through an integrated approach of biochemical, molecular and cellular methods, we defined the direct physical interactions between Nrp-1 and integrins. We have also extended this work to demonstrate the functional importance and contribution of the interactions in integrin-mediated cell adhesion on extracellular matrix (ECM) in angiogenesis and platelet function during wound healing and provide a molecular basis for the integration of Nrps/integrins in cell migration, adhesion to ECM, breast cancer initiation and breast cancer stem cell fate determination.

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Abe, Daniel Kanda. "Análise da expressão dos genes CD105 (endoglina), VEGF, VEGFR1 e VEGFR2 no carcinoma de células renais e correlação com fatores prognósticos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5153/tde-02102013-094530/.

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INTRODUÇÃO: A angiogênese tem sido proposta como um marcador de prognóstico em uma variedade de tumores incluindo o renal. No avanço da compreensão da biologia molecular do carcinoma de células renais (CCR) os genes CD105 (endoglina), VEGF, VEGFR1 e VEGFR2 são seletivamente expressos em células endoteliais vasculares sendo estudados como potenciais alvos terapêuticos. OBJETIVOS: Este estudo analisou a expressão destes quatro genes no tecido renal normal e CCR e suas correlações com os fatores prognósticos para a neoplasia. MÉTODOS: Os níveis de expressão de CD105, VEGF, VEGFR1 e VEGFR2 foram analisados por Reação da Transcriptase Reversa em tempo real (qRT-PCR) em amostras de tumor fresco congelado coletados de 56 pacientes submetidos à nefrectomia parcial ou radical por CCR. Neste estudo foram avaliados os níveis de expressão dos genes em tecidos normais e tumorais e comparados com fatores prognósticos como tamanho tumoral (> ou <= 7 cm), Grau de Fuhrman (1-2 e 3-4) e invasão microvascular (presente ou ausente). RESULTADOS: A análise dos quatro genes demonstrou que CD105 esta subexpresso em 94.7% dos casos e a superexpressão de VEGF, VEGFR1 e VEGFR2 ocorreu em 53,6%, 85,7% e 64,3% dos casos respectivamente. A expressão de endoglina foi significativamente maior em pacientes com doença metastática (p=0,05) em relação ao grupo sem metástases. Além disso, o gene do VEGFR2 foi associado com estadiamento T, apresentando uma média de expressão maior nos pacientes portadores de doença pT1-2 (p=0,04). CONCLUSÕES: Nossos experimentos demonstraram que a endoglina está subexpressa em carcinoma de células renais em relação com o tecido renal normal e a presença de níveis mais elevados está relacionada à doença metastática. Os genes VEGF, VEGFR1 e VEGFR2 encontram-se superexpressos no CCR e uma maior expressão do gene VEGFR2 está relacionada com estadiamento T1 e T2
INTRODUCTION: Angiogenesis has been proposed as a prognostic marker in a variety of human malignancies, including renal cancer. Due to a better understanding of the underlying biology of Renal Cell Carcinoma (RCC) the genes expression of CD105 (endoglina), VEGF, VEGFR1 and VEGFR2 that are selectively expressed in vascular endothelial cells are being studied as potential therapeutic targets. OBJECTIVES: This study analyzed the expression of these four genes in normal kidney tissue and RCC and relationship with prognostic factors. METHODS: CD105, VEGF, VEGFR1 and VEGFR2 expression levels were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) in fresh-frozen malignant tissue specimens collected from 56 patients submitted to radical or partial nephrectomy. This study assessed the expression of genes in normal and tumor tissues, and compared with classic prognostic parameters in CCRCC , such as tumor size (larger or smaller than 7 cm) Fuhrman grade (1-2 and 3-4) and microvascular invasion (this or absent). RESULTS: The analysis of these four genes showed that CD105 is subexpressed in 94.7% of cases and the overexpression of VEGF, VEGFR1 and VEGFR2 occurred in 53.6%, 85.7% and 64.3% of cases respectively in tumor tissues compared to controls. The expression of endoglin was significantly higher in patients with metastatic disease (p = 0.05). In addition, VEGFR2 gene was associated with stage T, with an average of expression higher in patients with stage T1-T2 (p = 0.040). Conclusions: These experiments demonstrated that endoglin was underexpressed in RCC compared to normal kidney and the presence of enhanced expression is associated with metastatic disease. VEGF, VEGFR1 and VEGFR2 were overexpressed in the CCRCC and a higher VEGFR2 expression was related with stage T1-2

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ORTEGA, NATHALIE. "Role de la biodisponibilite du vegf et des fonctions induites par chacun des recepteurs, vegfr1 et vegfr2, dans l'initiation du processus angiogenique." Toulouse 3, 1999. http://www.theses.fr/1999TOU30064.

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L'angiogenese est un processus invasif, aboutissant a la formation de nouveaux vaisseaux a partir de vaisseaux preexistants. Le facteur primordial de ce processus est le vegf (vascular endothelial growth factor). Il existe sous six isoformes qui different par leur solubilite et leurs activites biologiques. L'isoforme de 189 acides amines (v189) differe de l'isoforme 165 (v165) par la presence d'une sequence tres basique codee par l'exon 6. Deux recepteurs tyrosine kinase sont connus pour ces facteurs : vegfr1 et vegfr2. En comparant les activites biologiques de v165 et v189 nous avons montre la dualite du mode d'action de v189. Cette isoforme agit non seulement par les voies de vegfr1 et vegfr2 mais aussi par la voie du fgfr1 en liberant du fgf2 des matrices extracellulaires. Parmi dix composants de la matrice extracellulaire, nous avons pu identifier un site de retention commun pour le v189 et le fgf2, il s'agit du perlican. La presence de la sequence codee par l'exon 6 entraine donc la retention de v189 dans la matrice extracellulaire et lui confere la capacite d'agir indirectement par liberation d'autres facteurs basiques. Pour determiner les fonctions des recepteurs, nous avons developpe des anticorps anti-idiotypes du vegf. Nous avons obtenu des agonistes specifiques du vegfr2. In vitro, ces anticorps induisent la phosphorylation du vegfr2, la proliferation mais pas la migration des cellules endotheliales. In vivo, ils stimulent l'angiogenese tumorale sans affecter les cellules endotheliales quiescentes. Dans un modele d'angiogenese corneenne les anti-idiotypes induisent une reponse angiogenique meme en absence de vegf. Ces resultats permettent d'identifier le vegfr2 comme etant un marqueur fonctionnel de cellules endotheliales engagees dans un processus angiogenique. La conversion phenotypique des cellules endotheliales semble independante du vegf lui-meme.

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Benke, Emily Marie. "Role of VEGF-C in Proliferation and Migration in a Cancer Model." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1533.

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Head and neck cancer ranks high among the most common cancers world wide. In addition, there is a high recurrence rate, as well as a high prevalence of loco-regional tumor spread. Among many factors contributing to metastasis is vascular endothelial cell growth factor C. VEGF-C is primarily an inducer of new lymph vessel formation, typically during embryogenesis; however, some advanced cancers show a significant increase in VEGF-C expression, suggesting a role in metastasis. In the current study, the effects of VEGF-C expression were tested in HN12 cells, which are highly metastatic and known to express high levels of the chemokine CXCL5. A connection between VEGF-C and CXCL5 expression was made in previous studies. VEGF-C expression was downregulated or upregulated in appropriate target cells, in order to test its effect on proliferation and migration. Downregulation of VEGF-C in HN12 cells resulted in a decrease in proliferation, migration and motility. Conversely, upregulation of VEGF-C in HN4 cells led to an increase in cell proliferation. In addition, downregulation of VEGF-C significantly lowered tumorigenicity in athymic mice. All results suggest VEGF-C is contributing to an increase in proliferation, migration and motility in this HNSCC model system.

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

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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.

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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.

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Guimarães, Carina de Fátima. "Expressão de VEGF (VEGFR1/VEGFR2) e avaliação estereológica da membrana corioalantóide a termo em éguas Puro Sangue Inglês: influência da pluriparidade sobre o peso dos potros ao nascimento." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/10/10131/tde-19022014-115000/.

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A interação materno fetal na espécie equina depende exclusivamente da complexidade anatômica e fisiológica da placenta e este órgão endócrino provisório é a peça chave do presente estudo, onde objetivou-se avaliar a influência do número de partos sob a eficiência placentária. Buscando, por meio da morfometria das macro e microrregiões, além da expressão do VEGF, VEGFR-1/Flt-1 e VEGFR-2/FLK-1 na membrana corioalantóide a termo, dados referentes à inter-relação da pluriparidade, contato materno fetal e peso dos neonatos da raça Puro Sangue Inglês. O delineamento experimental consistiu em um estudo analítico, observacional, transversal, prospectivo. Foram acompanhados cinquenta partos de éguas divididas em três grupos de acordo com a pluriparidade: primíparas (n=18), 2 a 5 partos (n=14) e 6 a 10 partos (n=18). Foram coletados e fixados em formol fragmentos de 3 cm2 das regiões do corpo do útero (Cut), corno uterino gestante (CG) e corno uterino contralateral (CnG) da membrana corioalantóide a termo pós delivramento. Após processamento foram corados pela técnica de Hematoxilina & Eosina e Picro-Sirus-Red. Os estudos imunohistoquímico (método avidina-biotina) e esterológico foram realizados ao microscópio óptico. Foram correlacionados número de partos, altura e perímetro torácico (PT) maternos; idade, altura e PT paternos; composição volumétrica dos compartimentos placentários juntamente com as áreas de superfície de contato materno-fetal e peso, altura e escore de vitalidade neonatal. A paridade, além de diretamente relacionada ao peso do neonato, demonstrou na avaliação morfofuncional ser determinante ao ganho de eficiência placentária. As membranas corioalantóides das éguas pluríparas tenderam a apresentar maior volume total no CG, aumento na porcentagem e volume total de vilos, além de maior densidade microcotiledonária e expressão do VEGF na região do CG. Entre as muitas correlações determinadas no grupo primíparas as mais relevantes foram peso da membrana com variáveis neonatais como peso (r=0,598), PT (r=0,775), tempo para mamar (r=0,553) e tempo de gestação (r=-0,527), além do PT da mãe com o tempo para ruptura do cordão umbilical (r=0,564), reflexo de sucção (r=0,625), para levantar (r=0,756) e decúbito esternal (r=-590). Da mesma forma no grupo 2 a 5 partos, neonatos que nasceram com maior peso, altura, e PT apresentaram menor tempo para levantar (r=-0,546; r=-0,869, r=-0,892), eliminação do mecônio (r=-0,535) e ruptura do cordão umbilical (r=-0,528; r=-0,881). Assim como no grupo 6 a 10 partos, o peso do potro apresentou correlação com o peso (r=0,793), PT (r=0,716) e altura (r=0,667) materna. O volume total do CG correlacionou com volume total do parênquima (r=-0,816) e epitélio nos vilos placentários do CG (r=-0,915), tempo de gestação (r=-0,483), tempo para reflexo de sucção (r=-0,672), para mamar (r=-0,525), e para eliminação do mecônio (r=-0,525). No que diz respeito às variáveis paternas, o peso paterno correlacionou com o volume total do parênquima nos vilos placentários do CnG (r=0,393) , além do PT do garanhão com o peso (r=0,316) e PT (r=0,425) do potro e volume total do CG (r=0,319). Desta forma, acredita-se que estes resultados possam fornecer ferramentas práticas para auxiliar na escolha das fêmeas e machos mais indicados para geração de potros neonatos com desenvolvimento adequado.
Fetomaternal interaction in equine species depends exclusively on the complexity of placental anatomy and physiology. This transient endocrine organ is the key of the present study, which aimed to evaluate the influence of parity on placental efficiency. Morphometric of macro and micro regions, expression of VEGF, VEGFR-1/Flt-1 and VEGFR-2/FLK-1 in term corioallantois were performed and data regarding parity, fetomaternal contact and neonatal weight were evaluated in Thoroughbred. The experimental study consisted of an analytical, observational, cross-sectional, prospective study. Fifty deliveries were monitored in mares divided into three groups according to parity: nulliparous (n=18), 2 to 5 deliveries (n=14) and 6 to 10 deliveries (n=18). Tissue sections measuring 3 cm 2 were collected and fixed in formol saline from term chorioallantois regions: uterine body (UtB), pregnant uterine horn (PH) and contralateral uterine horn (CtH). After processing, samples were stained using Hematoxylineosin and Picro-Sirus-Red. Imunnohistochemistry (avidin-biotin method) and stereology were performed using an optic microscope. Correlations between parity, maternal height and thoracic perimeter; paternal age, height and thoracic perimeter; volume composition of placental compartments, surface area of fetomaternal contact and weight, height and neonatal vitality score were performed. Parity was directly related to weight of the neonate and demonstrated in morphofunctional evaluation to be determinant for placental efficiency. Chorioallantoic membranes from pluriparous mares tended to have greater total PH volume, higher percentage and total villi volume, and greater microcotiledonary density and VEGF expression in PH region. There were several correlations found in nulliparous group, the most relevant were membrane weight and neonatal parameters such as weight (r=0,598), thoracic perimeter (r=0,775), time to nurse (r=0,553) and gestational length (r=-0,527) and also mares thoracic perimeter with time to rupture the umbilical cord (r=0,564), suckle reflex (r=0,625), time to stand (r=0,756) and to achieve sternal recumbency (r=-590). Likewise, for the 2 to 5 deliveries group, neonates that were born heavier, taller and with greater thoracic perimeter took less time to stand (r=-0,546; r=-0,869, r=-0,892), pass meconium (r=-0,535) and rupture the umbilical cord (r=-0,528; r=-0,881). In the group of mares between 6 and 10 deliveries, foals weight was correlated to maternal weight (r=0,793), thoracic perimeter (r=0,716) and height (r=0,667). Total PH volume correlated to total parenchyma (r=-0,816) and epithelium in placental villi in PH (r=-0,915), gestational lenght (r=-0,483), time to suckle reflex (r=- 0,672), to nurse (r=-0,525), and pass meconium (r=-0,525). Regarding Paternal variables, paternal weight correlated to total parenchyma volume in placental villi of the CtH (r=0,393). Also thoracic perimeter of the stallion correlated to neonatal weight (r=0,316) thoracic perimeter (r=0,425) and total volume of the PH (r=0,319). Therefore, these data provides rationale for an adequate choice of mares and stallions to generate well-developed neonates.

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Schmidt, Augusto Frederico Santos. "Efeiro do tratamento pré-natal com ácido retinóico na expressão pulmonar de VEGF e seus receptores VEGFR1 e VEGFR2 no modelo animal de hérnia diafragmática congênita induzida pelo nitrofen." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310453.

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Orientador: Lourenço Sbragia Neto
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-16T01:31:04Z (GMT). No. of bitstreams: 1 Schmidt_AugustoFredericoSantos_D.pdf: 2455947 bytes, checksum: 2419510f01584a15bbc44f3555be5714 (MD5) Previous issue date: 2010
Resumo: A hérnia diafragmática congênita (HDC) é uma doença grave com alta mortalidade devido à hipoplasia e hipertensão pulmonar. A via do ácido retinóico tem sido implicada na patogênese da HDC e pode ser uma alternativa de intervenção na promoção da alveolarização e vascularização pulmonar. O fator de crescimento vascular do endotélio (VEGF - Vascular Endothelial Growth Factor) e seus receptores VEGFR1 e VEGFR2 têm importante função no crescimento e na vascularização pulmonar, e, possivelmente, na patogênese da HDC. No entanto, não se conhece como o tratamento pré-natal com ácido retinóico pode afetar a vascularização pulmonar e seus fatores de crescimento. O objetivo deste estudo foi analisar o efeito do tratamento pré-natal com ácido retinóico na vascularização pulmonar e na expressão pulmonar de VEGF e seus receptores VEGFR1 e VEGFR2 em fetos de rato com HDC induzida pelo nitrofen (2,4-dicloro-4'nitrodifenil éter). Fetos de ratas Sprague-Dawley prenhes foram divididos em oito grupos: 1) controle externo, 2) placebo óleo nitrofen; 3) placebo óleo ácido retinóico, 4) tratados com ácido retinóico, 5) expostos ao nitrofen sem HDC, 6) expostos ao nitrofen com HDC, 7) expostos ao nitrofen sem HDC e tratados com ácido retinóico, 8) expostos ao nitrofen com HDC e tratados com ácido retinóico. Nitrofen foi administrado por via oral (gavagem) com 9,5 dias de gestação. Ácido retinóico foi administrado por via intraperitoneal com 18,5, 19,5 e 20,5 dias de gestação na dose de 5 mg/kg/dia, a coleta fetal foi realizada com 21,5 dias (termo=22 dias). Cada grupo fetal foi composto por 25 fetos. As variáveis morfológicas estudadas foram: peso corporal (PC), peso pulmonar total (PPT), peso do pulmão esquerdo (PPE) e a relação peso pulmonar total / peso corporal (PPT/PC). A morfologia pulmonar foi estudada pela mensuração da média linear de interceptação (MLI) e seus componentes diâmetro interno dos espaços aéreos (DEA) e a relação de comprimento de transecção do parênquima / espaço aéreo (MCTP). A morfologia vascular foi estudada pela mensuração do diâmetro externo (DE), diâmetro interno (DI) e espessura proporcional da camada muscular média (ECM) de arteríolas pulmonares de resistência. A expressão de VEGF e dos receptores VEGFR1 e VEGFR2 foi analisada por meio de imunoistoquímica e western blotting. Os dados morfológicos e morfométricos foram analisados pelo teste ANOVA com pós-teste de Tukey-Kramer, a avaliação semiquantitativa da imunoistoquímica foi analisada pelo teste de Kruskal-Wallis com pós-teste de Dunn, sendo considerados significativos valores de p<0,05 para ambos os testes. A freqüência de HDC observada entre os fetos expostos ao nitrofen foi de 40%. As variáveis morfológicas apresentaram diminuição significativa nos grupos expostos ao nitrofen, especialmente nos fetos com HDC (p<0,05). O tratamento com ácido retinóico não alterou as variáveis morfométricas pulmonares. Fetos com HDC apresentaram aumento da ECM, enquanto o tratamento com ácido retinóico reduziu a ECM nos fetos com HDC (p<0.001). A presença de HDC levou à diminuição da expressão de VEGF, VEGFR1 e VEGFR2, enquanto o tratamento com ácido retinóico recuperou a expressão de VEGF e VEGFR1. A alteração sinalização da via do VEGF na HDC pode estar associada à patogênese da hipoplasia e da hipertensão pulmonar. O tratamento pré-natal com ácido retinóico pode fornecer vias para tratamento da hipertensão pulmonar na HDC por meio da redução da ECM das arteríolas pulmonares e recuperação do VEGF e seus receptores
Abstract: Congenital diaphragmatic hernia (CDH) is a life-threatening disease with high mortality due to the pulmonary hypertension and hypoplasia. Vascular endothelial growth factor (VEGF) and its receptors VEGFR1 and VEGFR2 play a major role in lung vascularization, growth, and possibly in the pathogenesis of CDH. However it is not know how prenatal treatment with retinoic acid can affect lung vascularization by acting on the VEGF signaling. The purpose of this study was to analyze the effect of antenatal retinoic acid treatment on the expression of pulmonary VEGF and its receptors VEGFR-1 and VEGFR-2 in rat fetuses with CDH induced by nitrofen. Fetuses from pregnant Sprague-Dawley rats (term=22 days) were divided in eight groups: 1) external control, 2) placebo oil nitrofen, 3) placebo oil retinoic acid, 4) treated with retinoic acid, 5) exposed to nitrofen without CDH, 6) exposed to nitrofen with CDH, 7) exposed to nitrofen without CDH and treated with retinoic acid, 8) exposed to nitrofen with CDH and treated with retinoic acid. Nitrofen (2,4- dichloro-4'-nitrodiphenyl ether) was administered by gavage (100 mg) at 9,5 days of gestation. Retinoic acid was administered intraperitoneally on days 18.5, 19.5 and 20.5 of gestation (5 mg/kg), harvest was performed at 21.5 days (term =22 days). Each fetal subgroup was composed of 25 fetuses. The morphologic variables studied were: body weight, total lung weight, left lung weight, and total lung weight to body weight ratio. Pulmonary morphometry was studied by measuring the mean linear intercept and its components: internal diameter of airspaces and mean transection length / airspace. Vascular morphometry was studied by measuring the external diameter, internal diameter and proportionate thickness of the medial muscular layer of pulmonary resistance arterioles. Immunohistochemistry and Western blotting analysis were used to assess VEGF, VEGFR-1 and VEGFR-2 expression. Data was analyzed using ANOVA with Tukey's post-test and immunohistochemistry was studied semiquantitatively using Kruskal-Wallis test with Dunn's post-test. The frequency of CDH was 40%. The morphological variables showed reduction in the nitrofen group with and without CDH, which were more pronounced in the latter (p<0.05). Retinoic acid did not affect fetal morphology. There was no difference in pulmonary morphometry among groups. Fetuses with CDH had increased proportionate thickness of the medial muscular layer of pulmonary arterioles, while treatment with retinoic acid reduced this variable in fetuses with CDH (p<0.001). Fetuses with CDH had reduced VEGF, VEGFR1 and VEGFR2 expression, while retinoic acid treatment restored expression VEGF and VEGFR1. VEGF signaling disruption may be associated with pulmonary hypertension in CDH. Retinoic acid may provide a pathway for acting on pulmonary hypertension by reducing medial thickness of pulmonary arterioles and restoring expression of VEGF and its receptors
Doutorado
Cirurgia
Doutor em Ciências da Cirurgia

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Veikkola, Tanja. "Dissecting VEGFR-2 and VEGFR-3 function : VEGFR-3 mediates lymphangiogenic signals." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/veikkola/.

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Patrić, A. S. Las Vegas for vegans. Melbourne: Transit Lounge Pub., 2012.

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Aasheim, Stein Peter. Vegard Ulvang. [Oslo]: Cappelen, 1993.

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Dûman, Huseyîn. Xeyala vegerê. Istanbul: Aram, 2020.

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Veger. Konak, İzmir: Weşanên Na, 2014.

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Sheehan, Jack. Las Vegas, southern Nevada: Hometown living Las Vegas style : Las Vegas stories. Houston: Pioneer Publications, 1992.

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Neimann, Greg. Las Vegas legends: What happened in Vegas... San Diego, CA: Sunbelt Publications, 2011.

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1940-2021, Hickey Dave, and Las Vegas Art Museum, eds. Vegas 360°: Panoramic photographs of Las Vegas. Las Vegas, Nev: Bright City Books, 2008.

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Rick, Browne, and Marshall James 1955-, eds. Planet Vegas: A portrait of Las Vegas. San Francisco: Collins Publishers, 1995.

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Las Vegas. Montréal: Libre expression, 2007.

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Michaels, Fern. Vegas sunrise. New York: Kensington Books, 1998.

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Farooqi, Ammad Ahmad, and 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.

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Escudier, Bernard, and 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.

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Roden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi, and Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings." In Critical Issues in Head and Neck Oncology, 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.

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Hansen, Truls Lynne. "Vegard, Lars." In Biographical Encyclopedia of Astronomers, 2226–27. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4419-9917-7_9371.

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Kim, Cheorl-Ho. "VEGFR–GM3 Interaction in Angiogenesis." In GM3 Signaling, 61–76. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5652-4_13.

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Choe, Hyojeong, and Steven H. Low. "Stabilized Vegas." In Advances in Communication Control Networks, 27–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-31597-1_2.

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Lugano, Roberta, Hua Huang, and Anna Dimberg. "Vascular Endothelial Growth Factor Receptor (VEGFR)." In Encyclopedia of Signaling Molecules, 5884–92. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101914.

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Lugano, Roberta, Hua Huang, and Anna Dimberg. "Vascular Endothelial Growth Factor Receptor (VEGFR)." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101914-1.

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Christie, Michael. "The Box of Vegies." In Discourse, Power, and Resistance Down Under, 45–56. Rotterdam: SensePublishers, 2013. http://dx.doi.org/10.1007/978-94-6209-509-0_5.

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Taylor, Sunaura. "Vegans, Freaks, and Animals." In The Disability Studies Reader, 337–42. 6th ed. 6th edition. | New York, NY : Routledge, 2021.: Routledge, 2021. http://dx.doi.org/10.4324/9781003082583-30.

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Тези доповідей конференцій з теми "VEGFRs"

Lee, Seung Hyeun, Eun Joo Lee, Gyu Young Hur, Sung Yong Lee, Sang Yeub Lee, Je Hyeong Kim, Chol Shin, et al. "Expression Of Vascular Endothelial Growth Factor (VEGF) And Vascular Endothelial Growth Factor Receptors (VEGFRs) In Lung Tissue Of Smokers And COPD Patients." 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.a2999.

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Fujita, Hidenori, Kazutaka Miyadera, Kimihiro Ito, Toru Takenaka, Jinhong Huang, Satoko Ito, Takamasa Suzuki, et al. "Abstract 3577: TAS-115: a highly potent c-Met + VEGFRs dual inhibitor with prominently safer profile." 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.am2011-3577.

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Kunii, Eiji, Hiroaki Ozasa, Tetsuya Oguri, Ken Maeno, Osamu Takakuwa, Takehiro Uemura, and Niimi Akio. "Abstract 3723: TAS-115, a novel MET + VEGFRs dual inhibitor, decreases the cytotoxic anticancer drug resistance in lung cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3723.

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Kato, Masanori, Hidenori Fujita, Kazutaka Miyadera, Yayoi Fujioka, Hiroaki Ochiiwa, Jinhong Huang, Kimihiro Ito, et al. "Abstract A245: TAS-115, a novel potent dual MET/VEGFRs inhibitor, has highly safer profile leading to more potent efficacy in vivo." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a245.

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Stepanova, Victoria, Padma Sheela Jayaraman, Sergei V. Zaitsev, Tatiana Lebedeva, Rachael M. Kershaw, and Douglas B. Cines. "Abstract 4164: uPA modulates angiogenesis through transcriptional regulation of vascular endothelial growth factor (VEGF) receptors VEGFR1 and VEGFR2." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4164.

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de La Motte Rouge, Thibault, Roger Mouawad, Eva Comperat, Jean-Christophe Thery, Stephane Vignot, Morgan Roupret, Jean-Philippe Spano, and 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.

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

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Jin, Younggeon, Juyoun Jin, Heekyoung Yang, Minjae Park, Weon Sup Lee, Sung-Woo Kim, Sang Ryeol Shim, et al. "Abstract 647: TTAC-0001, anti-VEGFR2/KDR monoclonal antibody, inhibits VEGFR signaling and tumor growth in preclinical models." 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.am2011-647.

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

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Jain, Sarika, Maureen M. Ward, Jennifer O'Loughlin, Marissa A. Boeck, Naomi Wiener, Ellen Chuang, Tessa Cigler, et al. "Abstract 4720: Incremental increase in VEGFR1+ and VEGFR2+ hemangiogenic progenitor cells predict relapse and tumor response in breast cancer (BC) patients." 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.am2011-4720.

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Звіти організацій з теми "VEGFRs"

Puttagunta, S. Retrofitting Vegas: Implementing Energy Efficiency in Two Las Vegas Test Homes. Office of Scientific and Technical Information (OSTI), April 2013. http://dx.doi.org/10.2172/1076649.

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Puttagunta, S. Retrofitting Las Vegas. Implementing Energy Efficiency in Two Las Vegas Test Homes. Office of Scientific and Technical Information (OSTI), April 2013. http://dx.doi.org/10.2172/1219999.

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Boyle, M. Business profile of metropolitan Las Vegas. Office of Scientific and Technical Information (OSTI), June 1988. http://dx.doi.org/10.2172/137584.

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

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Анотація:

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.

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Piechota, Thomas C. Resource Conservation and a Sustainable Las Vegas. Office of Scientific and Technical Information (OSTI), May 2014. http://dx.doi.org/10.2172/1134043.

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Kearney, Joseph B., and Victoria L. Bautch. Flt-1 (VEGFR-1) as an Angiogenic Inhibitor: Implications for a Novel Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417967.

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Milbrath, Brian D., Matthew W. Cooper, Lance S. Lidey, Ted W. Bowyer, James C. Hayes, Justin I. McIntyre, L. Karr, D. Shafer, and J. Tappen. Atmospheric Radioxenon Measurements in North Las Vegas, NV. Office of Scientific and Technical Information (OSTI), July 2006. http://dx.doi.org/10.2172/890734.

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Boyle, M. Current target industry analysis: Las Vegas Metropolitan Area. Office of Scientific and Technical Information (OSTI), June 1988. http://dx.doi.org/10.2172/137580.

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None, None. The New American Home 2004 Las Vegas, Nevada. Office of Scientific and Technical Information (OSTI), December 2003. http://dx.doi.org/10.2172/1217981.

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Rodgers, A., H. Tkalcic, and D. McCallen. The Las Vegas Valley Seismic Response Project: Ground Motions in Las Vegas Valley from Nuclear Explosions at the Nevada Test Site. Office of Scientific and Technical Information (OSTI), March 2005. http://dx.doi.org/10.2172/15015168.

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