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Cited by 2 publications
(5 citation statements)
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“…It has been shown that the inactivation of the NF1 gene in this cell lineage in mice was both sufficient and necessary to cause neointima formation and evidence of vascular inflammation similar to that observed in NF1 knockout mice. 29 Although the manifestations of NF1 vasculopathy are mostly arterial, patients may also present with venous rupture, venous aneurysms, and/or VT. [8][9][10][11][12]31 It has been shown that the absence of NF1 in vitro is sufficient for human venous endothelium cells to undergo autonomous proliferation. 28 This endothelial dysfunction has been extensively implicated in the pathogenesis of VT. [32][33][34][35] In this setting, the venous endothelium also shows altered vascular morphogenesis, which helps to explain the vascular morphological alterations in NF1 patients (that is, stenosis and aneurysms), 6,9,12,14,19,31 some of which may further increase the risk of VT (that is, venous aneurysm).…”
Section: Discussionmentioning
confidence: 99%
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“…It has been shown that the inactivation of the NF1 gene in this cell lineage in mice was both sufficient and necessary to cause neointima formation and evidence of vascular inflammation similar to that observed in NF1 knockout mice. 29 Although the manifestations of NF1 vasculopathy are mostly arterial, patients may also present with venous rupture, venous aneurysms, and/or VT. [8][9][10][11][12]31 It has been shown that the absence of NF1 in vitro is sufficient for human venous endothelium cells to undergo autonomous proliferation. 28 This endothelial dysfunction has been extensively implicated in the pathogenesis of VT. [32][33][34][35] In this setting, the venous endothelium also shows altered vascular morphogenesis, which helps to explain the vascular morphological alterations in NF1 patients (that is, stenosis and aneurysms), 6,9,12,14,19,31 some of which may further increase the risk of VT (that is, venous aneurysm).…”
Section: Discussionmentioning
confidence: 99%
“…[40][41][42] It has been reported once in the setting of NF1, by an exostosis, in the popliteal vein. 10 One study 43 conducted with patients harboring high-grade non-Hodgkin lymphoma showed that venous compression by the tumor was present in 51% of patients with DVT. Given the higher prevalence of neurofibromas in NF1 patients, it is thus reasonable to assume that DVT secondary to tumoral compression may also have a higher prevalence in this population.…”
Section: Discussionmentioning
confidence: 99%
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