Bevacizumab efficacy in treatment of brain radiation necrosis

2019 ◽  
Vol 1 (10) ◽  
pp. 15-21
Author(s):  
O. V. Absalyamova ◽  
G. L. Kobiakov ◽  
S. L. Gutorov ◽  
E. R. Vetlova ◽  
S. V. Zolotova ◽  
...  
Keyword(s):  
Adverse Effect ◽  
Vascular Endothelial Growth Factor ◽  
Arteriovenous Malformations ◽  
Radiation Necrosis ◽  
Critical Role ◽  
Common Adverse Effect ◽  
Vascular Endothelial ◽  
Brain Radiation Necrosis ◽  
Endothelial Growth Factor ◽  
Brain Radiation

Radiation therapy (RT) plays an important role in treatment of primary and metastatic CNS tumors and some non-neopiastic conditions (arteriovenous malformations, trigeminal neuralgia). Radiation necrosis (RN) is a common adverse effect of RT. Until recently steroid therapy was used as a main treatment regimen for RN. Mechanisms of RN development are not clear; however, it was shown that vascular endothelial growth factor (VEGF) plays a critical role in its formation. A number of surveys showed efficacy of bevacizumab as an anti-VEGF agent in treatment of RN. Radiation necrosis pathogenesis, diagnostics and treatment are summarized in this review.

scholarly journals Role of Vascular Endothelial Growth Factor (VEGF) in Human Embryo Implantation: Clinical Implications

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 253
Author(s):  
Xi Guo ◽  
Hong Yi ◽  
Tin Chiu Li ◽  
Yu Wang ◽  
Huilin Wang ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Recurrent Miscarriage ◽  
Embryo Implantation ◽  
Critical Role ◽  
Angiogenic Factor ◽  
Vascular Endothelial ◽  
Underlying Mechanisms ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the developing embryo and the endometrium. There is a correlation between the alteration of VEGF expression and reproductive failure, including recurrent implantation failure (RIF) and recurrent miscarriage (RM). In order to clarify the role of VEGF in embryo implantation, we reviewed recent literature concerning the expression and function of VEGF in the reproductive system around the time of embryo implantation and we provide a summary of the findings reported so far. We also explored the effects and the possible underlying mechanisms of action of VEGF in embryo implantation.

scholarly journals An Update on Medications for Brain Arteriovenous Malformations

Neurosurgery ◽  
2020 ◽  
Vol 87 (5) ◽  
pp. 871-878
Author(s):  
Daniel M S Raper ◽  
Ethan A Winkler ◽  
W Caleb Rutledge ◽  
Daniel L Cooke ◽  
Adib A Abla
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Clinical Trials ◽  
Arteriovenous Malformations ◽  
Treatment Options ◽  
Vascular Endothelial ◽  
Brain Arteriovenous Malformations ◽  
Disease States ◽  
Current State ◽  
Endothelial Growth Factor

Abstract Despite a variety of treatment options for brain arteriovenous malformations (bAVMs), many lesions remain challenging to treat and present significant ongoing risk for hemorrhage. In Vitro investigations have recently led to a greater understanding of the formation, growth, and rupture of bAVMs. This has, in turn, led to the development of therapeutic targets for medications for bAVMs, some of which have begun testing in clinical trials in humans. These include bevacizumab, targeting the vascular endothelial growth factor driven angiogenic pathway; thalidomide or lenalidomide, targeting blood-brain barrier impairment; and doxycycline, targeting matrix metalloproteinase overexpression. A variety of other medications appear promising but either requires adaptation from other disease states or development from early bench studies into the clinical realm. This review aims to provide an overview of the current state of development of medications targeting bAVMs and to highlight their likely applications in the future.

scholarly journals Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

2000 ◽  
Vol 74 (22) ◽  
pp. 10699-10706 ◽  
Author(s):  
Loreen J. Savory ◽  
Steven A. Stacker ◽  
Stephen B. Fleming ◽  
Brian E. Niven ◽  
Andrew A. Mercer
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Virus Infection ◽  
Vascular Endothelial Cells ◽  
Critical Role ◽  
Skin Lesions ◽  
Orf Virus ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

ABSTRACT Infection by the parapoxvirus orf virus causes proliferative skin lesions in which extensive capillary proliferation and dilation are prominent histological features. This infective phenotype may be linked to a unique virus-encoded factor, a distinctive new member of the vascular endothelial growth factor (VEGF) family of molecules. We constructed a recombinant orf virus in which the VEGF-like gene was disrupted and show that inactivation of this gene resulted in the loss of three VEGF activities expressed by the parent virus: mitogenesis of vascular endothelial cells, induction of vascular permeability, and activation of VEGF receptor 2. We used the recombinant orf virus to assess the contribution of the viral VEGF to the vascular response seen during orf virus infection of skin. Our results demonstrate that the viral VEGF, while recognizing a unique profile of the known VEGF receptors (receptor 2 and neuropilin 1), is able to stimulate a striking proliferation of blood vessels in the dermis underlying the site of infection. Furthermore, the data demonstrate that the viral VEGF participates in promoting a distinctive pattern of epidermal proliferation. Loss of a functional viral VEGF resulted in lesions with markedly reduced clinical indications of infection. However, viral replication in the early stages of infection was not impaired, and only at later times did it appear that replication of the recombinant virus might be reduced.

scholarly journals Possible co-option of a VEGF-driven tubulogenesis program for biomineralization in echinoderms

2019 ◽  
Author(s):  
Miri Morgulis ◽  
Tsvia Gildor ◽  
Modi Roopin ◽  
Noa Sher ◽  
Assaf Malik ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Sea Urchin ◽  
Regulatory Networks ◽  
Critical Role ◽  
Vascular Endothelial ◽  
Upstream Gene ◽  
Vegf Signaling ◽  
Vegf Pathway ◽  
Endothelial Growth Factor

AbstractBiomineralization is the process in which living organisms use minerals to form hard structures that protect and support them. Biomineralization is believed to have evolved rapidly and independently in different phyla utilizing existing components used for other purposes. The mechanistic understanding of the regulatory networks that drive biomineralization and their evolution is far from clear. The sea urchin skeletogenesis is an excellent model system for studying both gene regulation and mineral uptake and deposition. The sea urchin calcite spicules are formed within a tubular cavity generated by the skeletogenic cells under the control the vascular endothelial growth factor (VEGF) signaling. The VEGF pathway controls tubulogenesis and vascularization across metazoans while its regulation of biomineralization was only observed in echinoderms. Despite the critical role of VEGF signaling in sea urchin spiculogenesis, the downstream program it activates was largely unknown. Here we study the cellular and molecular machinery activated by the VEGF pathway during sea urchin spiculogenesis and reveal multiple parallels to the regulation of tubulogenesis during vertebrate vascularization. Human VEGF rescues sea urchin VEGF knock-down; VEGF-dependent vesicle deposition plays a significant role in both systems and sea urchin VEGF signaling activates hundreds of genes including biomineralization and vascularization genes. Five upstream transcription factors and three signaling genes active in spiculogenesis are homologous to vertebrate factors that regulate vascularization. Overall, our findings suggest that sea urchin spiculogenesis and vertebrate vascularization diverged from a common ancestral tubulogenesis program, broadly adapted for vascularization and specifically co-opted for biomineralization in the echinoderm phylum.Significance statementThe sea urchin calcite spicules and vertebrate blood vessels are quite distinct in their function, yet both have a tubular structure and are controlled by the vascular endothelial growth factor (VEGF) pathway. Here we study the downstream program by which VEGF pathway drives sea urchin spiculogenesis and find remarkable similarities to the control of vertebrate vascularization. The similarities are observed both in the upstream gene regulatory network, in the downstream effector genes and the cellular processes that VEGF signaling controls at the site of the calcite spicule formation. We speculate that sea urchin spiculogenesis and vertebrate vascularization diverged from a common ancestral tubulogenesis program that was co-opted for biomineralization in the echinoderm phylum.

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