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The evolution of the packing of postnasal space following transpalatal excision of JNA in the last 7 decades is described and a modification is presented for minimizing the immediate postoperative morbidity. [ABSTRACT FROM AUTHOR]

Background: The molecular profile of juvenile nasopharyngeal angiofibroma (JNA) is extremely variable. In absence of established molecular signature the molecular targeting seems difficult for this heterogeneous disease. To establish a basic molecular signature, this paper analyses the interaction of 7 markers according to their ranks as per the decreasing scale of molecular expression.Materials and methods: Fourteen samples of JNA were obtained following surgical excision and mRNA expressions were established through real-time polymerase chain reaction (RT-PCR) for vasculoendothelial growth factor (VEGF), fibroblastic growth factor (FGF), c-Kit, c-myc, Ras, platelet-derived growth factor (PDGF) and tumor suppressor gene p53. Nasal polyp was taken as control. The quantitative expressions for every marker were ranked on a decreasing scale and were compared by Spearman's rank correlation test to define the statistically significant interaction. An attempt was also made to overview the basic clinical parameters (age, duration of symptoms, radiological staging, intraoperative haemorrhage and tumor-volume/weight) associated with enhanced molecular expressions for every marker. Results: Five significant molecular interactions were identified on the basis of rank-correlation: (1) FGF/VEGF (p < 0.01); (2) Ras/FGF (p < 0.01); (3) Ras/VEGF (p < 0.001), (4) FGF/c-Kit (p < 0.05); (5) c-Myc/p53 (p < 0.05). These basic 'molecular signatures' suggested a preliminary 'molecular classification'. The implication of the interactions between FGF, VEGF and Ras were the most outstanding observation that not only revealed a direct relationship but were also consistent with the clinical behaviour. In addition, a non-significant interaction was identified with c-Myc/PDGF and also an inverse relationship between FGF/c-Kit.Conclusions: FGF, VEGF, and Ras being significantly interrelated seemed to be the 'most soft' molecular targets for JNA. The other targets observed included FGF/c-Kit and c-Myc/p53 interactions that seemed equally important but only after VEGF/FGF/Ras complex per se. These preliminary signatures are likely to provide a background for further expansion of the molecular classification of JNA. [ABSTRACT FROM AUTHOR]

Background: The histological and electron-microscopic (EM) characteristics of juvenile nasopharyngeal angiofibroma (JNA) have been described but no study has compared them with one another or with clinical features. The objective is to compare ultrastructural characteristics of JNA with clinical parameters. Methods: This prospective study included histology of 21 samples of which only 13 underwent transmission-EM. Four clinical parameters (age, duration, epistaxis, recurrence), three radiological-staging, 13 histological and 15 EM characteristics were considered. A descriptive analysis for association of these characteristics and also with clinical parameters was attempted. Furthermore statistical analysis of clinical and radiological categories with respect to frequencies of ultrastructural characteristics was also undertaken. Results: Dense-intranuclear-inclusions (DNI) and peripheral-nuclear-irregularities were universally encountered while other very prominent features were nuclear-blebs-and-pockets, myoid-features, thin-vessel-wall (TnVW), irregular-vascular-contour (IVC) and fibrous-stroma (FS). Statistical significance was obtained between recurrence with histology (p = 0.04) and Fisch staging with EM (p = 0.001). While muscle-in-vessel-wall, thick-vessel-wall, mast-cells, stellate-stromal-cells and cellular-stroma predominated in recurrent cases, the upfront disease showed predominance of scar-like-stroma, fusiform-stromal-cells, IVC, TnVW, FS, organised-collagen-bundles and less-cellular-stroma. A very unique Rod-like-structures were appreciated in the cytoplasm of the fibroblast for the first time. Conclusions: While histological parameters of recurrence need further validation, a larger sample may better define histopathological surrogate for predicting intracellular dynamics that may further correlate with underlying cellular stresses. Hence an 'ultrastructural staging' may better customise treatment protocol and prognosis. Furthermore 'characteristic' unique rods need to be further investigated along with validation of viral aetiology for DNI. [ABSTRACT FROM AUTHOR]