Background: Angiogenesis and lymphogenesis which were promoted by vascular endothelial growth factor (VEGF) and VEGF-C are important in the growth and metastasis of solid tumors. The high level of VEGF and VEGF-C were distributed in numerous types of cancers, but their distribution and expression in Wilms tumor, the most common pediatric tumor of the kidney, was unclear.
Methods: To learn about the distribution, mass spectroscopy and immunohistochemistry were used to measure the level of VEGF and VEGF-C in serum and tissue of Wilms tumor.
Results: The expression level of VEGF in serum of Wilms tumor was the same as in pre-surgery and control, so it was the same case of VEGF-C. Both of these factors were chiefly located in Wilms tumor tissue, but not in borderline and normal. In addition, the higher clinical staging and histopathologic grading were important elements in high expression of VEGF and VEGF-C. Gender, age and the size of tumor have not certainly been implicated in expression level of VEGF and VEGF-C.
Conclusions: The lymph node metastasis and growth of tumors resulted from angiogenesis and lymphogenesis which were promoted by VEGF and VEGF-C in Wilms tumor. The autocrine and paracrine process of VEGF and VEGF-C were the principal contributor to specific tissues of Wilms tumor but not to the entire body.
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Transl Vis Sci Technol
December 2024
Opthea Limited, Melbourne, Victoria, Australia.
Purpose: Sozinibercept inhibits vascular endothelial growth factors (VEGFs) C and D. This study evaluated outcomes following switching from anti-VEGF-A monotherapy to intravitreal injections of three dose levels of sozinibercept in combination with aflibercept in patients with diabetic macular edema (DME).
Methods: A phase 1b, open-label, multicenter dose-escalation study with a 24-week follow-up.
Kidney360
December 2024
Department of Medical Physiology, Texas A&M University School of Medicine, Bryan, TX 77807, USA.
Background: Chronic kidney disease (CKD) counts acute kidney injuries (AKI) as one of its many underlying causes. Lymphatic vessels are important in modulating inflammation post-injury. Manipulating lymphatic vessel expansion thus has the potential to alter CKD progression.
View Article and Find Full Text PDFMol Biol Rep
December 2024
Humanitas College, Kyung Hee University, 1732 Deogyeongdae-Ro, Yongin, 17104, South Korea.
Background: Secondary lymphedema is a progressive condition caused by lipid- and protein-rich interstitial fluid accumulation resulting from compromised lymphatic function. It commonly occurs in cancer patients following surgical lymph node ablation and radiation treatment. This study aims to elucidate the effects of exercise on the myokine interleukin (IL)-6 and the molecular changes involved in lymphangiogenesis and extracellular matrix (ECM) synthesis using a lymphedema mouse model.
View Article and Find Full Text PDFLymphatics
December 2024
Department of Pathology, Anatomy and Cell Biology and the Clinical and Translational Research Center of Excellence, Meharry Medical College, 1005 Dr. D.B. Todd Jr. Boulevard, Nashville, TN 37208, USA.
Inflammatory breast cancer (IBC) is characterized by numerous tumor emboli within lymphatics. In a recent study, we observed tumor embolic budding both in vitro and in vivo within lymphovascular spaces and proposed this to account for the plethora of tumor emboli seen in IBC. These observations did not address, however, how lymphovascular invasion is initiated or the mechanisms involved.
View Article and Find Full Text PDFJ Exp Med
February 2025
Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Cerebrospinal fluid (CSF), antigens, and antigen-presenting cells drain from the central nervous system (CNS) into lymphatic vessels near the cribriform plate and dura, yet the role of these vessels during stroke is unclear. Using a mouse model of ischemic stroke, transient middle cerebral artery occlusion (tMCAO), we demonstrate stroke-induced lymphangiogenesis near the cribriform plate, peaking at day 7 and regressing by day 14. Lymphangiogenesis is restricted to the cribriform plate and deep cervical lymph nodes and is regulated by VEGF-C/VEGFR-3 signaling.
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