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Milroy Disease
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
The FLT4 (FMS-like tyrosine kinase 4) gene on chromosome 5q35.3 is 48.7 kb in length with 31 exons and encodes a 1,363 aa, 152 kDa tyrosine-protein kinase (FLT4, also known as vascular endothelial growth factor receptor 3 [VEGFR3]), which is a lymphatic endothelial cell-specific receptor for vascular endothelial growth factors C (VEGFC) and D (VEGFD) [7].
How much pharmacological therapy can be incorporated in primary lymphedema management?
Published in Byung-Boong Lee, Peter Gloviczki, Francine Blei, Jovan N. Markovic, Vascular Malformations, 2019
The potential value of this approach has been shown using a mouse model of primary lymphedema of the Milroy type (caused by heterozygous inactivating missense mutations of the FLT4 gene, which regulates VEGFR3 expression) and virus-mediated VEGFC gene therapy (VEGFC is the natural ligand of VEGFR3).3 The gene therapy led to the generation of functional lymphatic vessels.
Angiogenesis in Hematological Malignancies
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
Alida C. Weidenaar, Hendrik J. M. de Jonge, Arja ter Elst, Evelina S. J. M. de Bont
NHL cells secrete VEGFA and express FLT1 and KDR, suggesting the presence of autocrine and paracrine pathways (105). Moreover, most of the malignant lymphomas express VEGFC, which can bind to FLT4 and is involved in lymph angiogenesis. The level of lymph vessel density (LVD) was significantly correlated to the expression levels of VEGFA and VEGFC.
A randomized, open-label, single-dose, two-cycle crossover study to evaluate the bioequivalence and safety of lenvatinib and Lenvima® in Chinese healthy subjects
Published in Expert Opinion on Investigational Drugs, 2022
Zhongnan Xu, Yanli Wang, Guangwen Liu, Jiahui Chen, Wanhua Wang, Yang Cheng, Qing Ren, Yingzi Cui, Wei Yang, Zhengzhi Liu, Xuesong Chen, Jinling Xue, Tianying Chang, Xinyao Qu, Shuang Yu, Yannan Zhou, Kaibo Xu, Zhengjie Su, Qiaohuan Deng, Yicheng Zhao, Haimiao Yang
Lenvatinib is an oral, multikinase inhibitor that targets the vascular endothelial growth factor receptors VEGFR1 (FLT1), VEGFR (KDR) and VEGFR3 (FLT4) [15]. Lenvatinib can also inhibit RTKs related to angiogenesis and carcinogenic pathways (including fibroblast growth factor (FGF) receptors FGFR 1–4, platelet-derived growth factor receptor α (PDGFRα), KIT and RET [16–18]. In the phase 3 randomized, double-blind, placebo-controlled, multicenter study of (E7080) lenvatinib for differentiated cancer of the thyroid (SELECT), lenvatinib significantly prolonged progression-free survival (PFS) in patients with progressive RR-DTC compared with placebo (18.3 versus 3.6 months) [19]. Based on the results of SELECT, lenvatinib monotherapy was approved for the treatment of RR-DTC in the United States, Europe and Japan [20,21]. In the 2017 National Comprehensive Cancer Network Clinical Practice Guidelines, lenvatinib was listed as the preferred treatment for progressive or symptomatic RR-DTC [6].
Detection of Pro- and Antiangiogenic Factors in the Human Sclera
Published in Current Eye Research, 2019
Simona L. Schlereth, Marcus Karlstetter, Deniz Hos, Mario Matthaei, Claus Cursiefen, Ludwig M. Heindl
In Table 1 and Figure 3, the results of all 96 tested factors are shown. Six more proangiogenic factors or factors that are involved in the structural integrity or maintenance of blood vessels were significantly downregulated in the human sclera compared to human conjunctiva: FLT4 (p = 1.52x10−4), (HGF) (p = 0.027), CD117 c-Kit (p = 0.033), PROX1 (p = 0.007), SEMA3F (p = 0.017) and TGFA (p = 0.001).
Fetal hydrops – a review and a clinical approach to identifying the cause
Published in Expert Opinion on Orphan Drugs, 2020
Esther Dempsey, Tessa Homfray, John M Simpson, Steve Jeffery, Sahar Mansour, Pia Ostergaard
Heterozygous mutations in the gene FLT4 (VEGFR3) cause Milroy disease, which typically presents at birth, or soon after, with bilateral pedal edema [126]. There have been rare reports of antenatal presentation of FLT4/VEGFR3 mutations, including fetuses affected by ascites, pleural effusions and limb edema [127–129].