Vascular endothelial growth factor signaling in development and disease

Karaman, Sinem; Leppänen, Veli-Matti; Alitalo, Kari

doi:10.1242/dev.151019

Cited by 259 publications

(205 citation statements)

References 115 publications

(135 reference statements)

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“…9 In this present study we could observe that VEGFR-2 IHC scores were significantly increased in sestamibi-positive adenomas compared to negative adenomas. 11 Moreover, activation of VEGFR-2 leads to endothelial cell proliferation, cell migration, and survival. 10 Its activation by the vascular endothelial growth factor-A (VEGF-A) induces angiogenesis via the formation of new blood vessels from preexisting vascular endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…VEGFR-2 is a major angiogenic tyrosine kinase receptor located on blood vessels. 11 Furthermore, the VEGF/VEGFR-2 signaling cascade controls cell 11 Moreover, activation of VEGFR-2 leads to endothelial cell proliferation, cell migration, and survival.…”

Section: Discussionmentioning

confidence: 99%

“…10 Its activation by the vascular endothelial growth factor-A (VEGF-A) induces angiogenesis via the formation of new blood vessels from preexisting vascular endothelial cells. 11 Moreover, activation of VEGFR-2 leads to endothelial cell proliferation, cell migration, and survival. 11 Furthermore, the VEGF/VEGFR-2 signaling cascade controls cell permeability 3 by modifying tyrosine kinase Src activation.…”

Section: Discussionmentioning

confidence: 99%

“…11 Moreover, activation of VEGFR-2 leads to endothelial cell proliferation, cell migration, and survival. 11 Furthermore, the VEGF/VEGFR-2 signaling cascade controls cell permeability 3 by modifying tyrosine kinase Src activation. 12 Our analysis of the expression profiles of VEGFR-2 in sestamibi-positive and -negative parathyroid adenomas suggest that sestamibi positivity may be linked to an increased permeability of the vessels to promote tumor cell growth.…”

Section: Discussionmentioning

confidence: 99%

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VEGFR‐2 is downregulated in sestamibi‐negative parathyroid adenomas

et al. 2019

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Background The purpose of this study was to determine the expression profile of several biomarkers in sestamibi‐positive (n = 23) and sestamibi‐negative (n = 6) parathyroid adenomas. Methods A tissue microarray of parathyroid adenomas from 29 patients was constructed and slides were stained for several proteins involved in angiogenesis, inflammation, cell adhesion, cell cycle, apoptosis, and with markers of the sonic hedgehog, mTOR, Forkhead box O and WNT signal transduction pathways. Protein expression was determined using an image‐analysis software (Spectrum Plus©, 38 Aperio). Results Protein expression analysis revealed that the vascular endothelial growth factor receptor 2 (VEGFR2) score was significantly higher in the sestamibi‐positive cohort compared to sestamibi‐negative adenomas (P = .038). Other proteins were not differentially expressed between sestamibi‐positive and sestamibi‐negative adenomas. Conclusion It is hypothesized that VEGFR‐2 overexpression in parathyroid adenomas increases vascular permeability resulting in a higher uptake of sestamibi.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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VEGFR‐2 is downregulated in sestamibi‐negative parathyroid adenomas

et al. 2019

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“…VEGF-A is the most potent angiogenic factor acting on VEGF receptor 2 (VEGFR2) in BECs [154]. VEGF-C and VEGF-D are crucial for the survival, proliferation, and migration of LECs by engaging VEGFR3 [155]. VEGF-A also influences lymphangiogenesis by recruiting immune cells (e.g., macrophages and mast cells) that produce VEGF-C and VEGF-D [9, 156].…”

Section: Mast Cells In Angiogenesis and Lymphangiogenesismentioning

confidence: 99%

Physiological Roles of Mast Cells: Collegium Internationale Allergologicum Update 2019

Varricchi

Rossi

Galdiero

et al. 2019

Int Arch Allergy Immunol

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Mast cells are immune cells which have a widespread distribution in nearly all tissues. These cells and their mediators are canonically viewed as primary effector cells in allergic disorders. However, in the last years, mast cells have gained recognition for their involvement in several physiological and pathological conditions. They are highly heterogeneous immune cells displaying a constellation of surface receptors and producing a wide spectrum of inflammatory and immunomodulatory mediators. These features enable the cells to act as sentinels in harmful situations as well as respond to metabolic and immune changes in their microenvironment. Moreover, they communicate with many immune and nonimmune cells implicated in several immunological responses. Although mast cells contribute to host responses in experimental infections, there is no satisfactory model to study how they contribute to infection outcome in humans. Mast cells modulate physiological and pathological angiogenesis and lymphangiogenesis, but their role in tumor initiation and development is still controversial. Cardiac mast cells store and release several mediators that can exert multiple effects in the homeostatic control of different cardiometabolic functions. Although mast cells and their mediators have been simplistically associated with detrimental roles in allergic disorders, there is increasing evidence that they can also have homeostatic or protective roles in several pathophysiological processes. These findings may reflect the functional heterogeneity of different subsets of mast cells.

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US FDA‐Approved Small‐Molecule Kinase Inhibitors for Cancer Therapy

Tadesse

Wang

2021

Burger's Medicinal Chemistry and Drug Discovery

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Abnormal activation of kinases is associated with various types of human cancer. A milestone approval of a small‐molecule kinase inhibitor (SMKI), imatinib, in 2001 for the treatment of chronic myeloid leukemia has revolutionized the clinical practice. This has invigorated the kinase‐targeted drug discovery and clinical sciences, and drug developers have been searching for the next revolutionary therapeutic agents to combat cancer. By mid‐2019, a total of 48 SMKIs have received their regulatory approvals from the United States Food and Drug Administration (USFDA) for the treatment of cancer. This article starts with an introduction of kinases; emphasis is placed on the differences between the structures of active and inactive kinases in that these structural disparities form the basis of the current classification of SMKIs which is subsequently outlined. Thereafter USFDA‐approved SMKI oncology drugs are delineated, with a great deal of attention paid to their respective oncology indications and co‐crystal structures with indication‐related kinases; an overview of biomedical rationales of the kinases being targeted is also provided. Towards the end, some of the current challenges and future prospects in developing SMKI‐based cancer therapies are discussed.

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Vascular endothelial growth factor signaling in development and disease

Cited by 259 publications

References 115 publications

VEGFR‐2 is downregulated in sestamibi‐negative parathyroid adenomas

VEGFR‐2 is downregulated in sestamibi‐negative parathyroid adenomas

Physiological Roles of Mast Cells: Collegium Internationale Allergologicum Update 2019

US FDA‐Approved Small‐Molecule Kinase Inhibitors for Cancer Therapy

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