2020
DOI: 10.1016/j.wneu.2020.07.208
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Immunohistochemical Profiles of Matrix Metalloproteinases and Vascular Endothelial Growth Factor Overexpression in the Antoni B Area of Vestibular Schwannomas

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Cited by 11 publications
(19 citation statements)
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“…The proteolytic activity of MMP-14 was related to the degree of SNHL in VS patients. (39)(40)(41) The expression of ADAM9 was higher in VS and related to functional impairment. (42,43)…”
Section: Proteasesmentioning
confidence: 99%
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“…The proteolytic activity of MMP-14 was related to the degree of SNHL in VS patients. (39)(40)(41) The expression of ADAM9 was higher in VS and related to functional impairment. (42,43)…”
Section: Proteasesmentioning
confidence: 99%
“…VEGF is one of the most prominent angiogenesis stimulator that can regulate irregular blood vessel sprouting and growth except for simple remodeling of the capillary basement membrane (65), and lead to development of an immuno suppressive tumor microenvironment (66). Compared with normal vestibular nerve, the expression of VEGF, VEGFR-1/Flt and VEGFR-2/Flk as well as the coreceptor NP1 were considerable increased in VS tissues, suggesting at least a part of neoplastic growth was induced via the promotion of angiogenesis (39,64,67). Tissue microarray analysis of 182 sporadic VSs found significantly higher VEGF levels in the groups of recurrent and preoperatively irradiated tumors when compared to primary VS patients (67).…”
Section: Rtksmentioning
confidence: 99%
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“…On the other hand, Antoni B cells are characterized by hypocellularity, loose microcystic tissue, and intratumoral microhemorrhage. The cystic component in schwannomas, represented by Antoni B cells, is highly consistent with the degree of cystic degeneration [2] . Cellular architecture is useful in explaining imaging features of cystic-dominant, solid-dominant, mixed-cystic, and solid schwannomas and the accompanying intratumoral hemorrhage or fluid-fluid level.…”
Section: Introductionmentioning
confidence: 66%
“…Charabi et al 31 reported that an increase in the size of cystic VSs may be caused by an expansion of the cystic component rather than by an actual increase in the number of tumor cells. However, Xia et al 32 recently conducted immunohistochemical studies of cystic and solid VSs and found that VEGF overexpression increased tumor vessel permeability and caused cyst fluid to leak from the fragile neovasculature, which in turn caused cystic expansion and intratumoral hemorrhage. Moreover, VEGF is known to promote tumor vascular permeability 33 .…”
Section: Discussionmentioning
confidence: 99%