Current molecular profile of juvenile nasopharyngeal angiofibroma: First comprehensive study from India

Pandey, Praveen; Mishra, Anupam; Tripathi, Anil Kumar; Verma, Vikas; Trivedi, Ritu; Singh, Hitendra Prakash; Kumar, Sunil; Patel, Brijesh R; Singh, Vinay Kumar; Pandey, Sushil; Pandey, Anshuman; Mishra, Subhash C.

doi:10.1002/lary.26250

Cited by 24 publications

(34 citation statements)

References 38 publications

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“…In addition, the roles of Toll-like receptors (TLR 3, TLR 7, TLR 9), cell-surface antigens (CD31, CD34, CD68, CD99), matrix metalloproteinases (MMP-1, MMP-2, MMP-9, MMP-14), and certain cytokines (IL-6, IL-17) were investigated [6,8,12,13,16,[36][37][38]. Of these, TLR 3 [8], CD34 [12], MMP 9 [36,37], IL-6, and IL-17 [6,38] were shown to be associated with JNA.…”

Section: Discussionmentioning

confidence: 99%

“…JNA-related molecular studies have focused on sex hormone receptors, with investigations being done of androgen receptors (AR), estrogen receptors (ER), and progesterone receptors (PR) [6,10,14,[18][19][20][21][22][23][24]39,40]. These studies indicated that AR is frequently expressed at high levels in cases of JNA [18][19][20][21][22].…”

Section: Literature Reviewmentioning

confidence: 99%

“…Therefore, vascular endothelial growth factor (VEGF), nerve growth factor (NGF), insulin-like growth factor (IGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and transforming growth factor (TGF) were assessed in many studies [2,5,6,10,12,[14][15][16]23,[25][26][27]. The levels of TGF-β1 [10,25,27,29], basic fibroblast growth factor (bFGF) [6,15,25,26], NGF (2), and VEGF [5,6,10,12,14,16,23,25] were found to be elevated in JNA. The most notable of which are TGF-β1 and VEGF.…”

Section: Literature Reviewmentioning

confidence: 99%

“…protooncogenes, including p53, c-Myc, H-Ras, Ki-Ras, c-Kit, p130Cas, Friend leukemia integration-1 (FLI-1), endoglin, podoplanin, stromelysin-3 (ST3), tenascin-C (TNC), syndecan-2, proliferating cell nuclear antigen (PCNA), Bcl-2, Ki-67, S-100, c-Fos, GSTM1 gene, AURKA, MDM2, Her-2/neu, and Hif-1 [2,[5][6][7][9][10][11][12][13][15][16][17]25,27,28,[32][33][34][35], in the etiology of JNA have been investigated. Among these, c-Myc [6,7,28], c-Kit (2,6,7), FLI-1 [5], endoglin [5,11], TNC [9], PCNA [10,12], Ki-67 [16], GSTM1 [17,33], AURKA and MDM2 (34) were shown to be associated with JNA.…”

Section: Literature Reviewmentioning

confidence: 99%

“…Among these, c-Myc [6,7,28], c-Kit (2,6,7), FLI-1 [5], endoglin [5,11], TNC [9], PCNA [10,12], Ki-67 [16], GSTM1 [17,33], AURKA and MDM2 (34) were shown to be associated with JNA. Among these, GSTM1-null genotype gene seems important.…”

Section: Literature Reviewmentioning

confidence: 99%

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Biomolecular Analysis of Juvenile Nasopharyngeal Angiofibroma

Mazlumoglu¹

2017

J Mol Genet Med

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Section: Discussionmentioning

confidence: 99%

Section: Literature Reviewmentioning

confidence: 99%

Section: Literature Reviewmentioning

confidence: 99%

Section: Literature Reviewmentioning

confidence: 99%

Section: Literature Reviewmentioning

confidence: 99%

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Biomolecular Analysis of Juvenile Nasopharyngeal Angiofibroma

Mazlumoglu¹

2017

J Mol Genet Med

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Inhibition of fibroblast growth factor receptor with AZD4547 mitigates juvenile nasopharyngeal angiofibroma

New

Jones

et al. 2017

Int Forum Allergy Rhinol

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Background Juvenile nasopharyngeal angiofibroma (JNA) is a benign tumor that presents in adolescent males. Although surgical excision is the mainstay of treatment, recurrences complicate treatment. There is a need to develop less invasive approaches for management. JNA tumors are composed of fibroblasts and vascular endothelial cells. We identified fibroblast growth factor receptor (FGFR) and vascular endothelial growth factor (VEGF) expression in JNA-derived fibroblasts. FGFR influences fibroblast proliferation and VEGF is necessary for angiogenesis. We hypothesized that targeting FGFR would mitigate JNA fibroblast proliferation, invasion, and migration, and that targeting the VEGF receptor would attenuate endothelial tubule formation. Methods After informed consent, fibroblasts from JNA explants of 3 patients were isolated. Fibroblasts were treated with FGFR inhibitor AZD4547, 0 to 25 µg/mL for 72 hours and proliferation was quantified using CyQuant assay. Migration and invasion of JNA were assessed using 24-hour transwell assays with subsequent fixation and quantification. Mitigation of FGFR and downstream signaling was evaluated by immunoblotting. Tubule formation was assessed in human umbilical vein endothelial cells (HUVECs) treated with vehicle control (dimethylsulfoxide [DMSO]) or semaxanib (SU5416) as well as in serum-free media (SFM) or JNA conditioned media (CM). Tubule length was compared between treatment groups. Results Compared to control, AZD4547 inhibited JNA fibroblast proliferation, migration, and invasion through inhibition of FGFR and downstream signaling, specifically phosphorylation of - p44/42 mitogen activated protein kinase (p44/42 MAPK). JNA fibroblast CM significantly increased HUVEC tubule formation (p = 0.0039). Conclusion AZD4547 effectively mitigates FGFR signaling and decreases JNA fibroblast proliferation, migration, and invasion. SU5416 attenuated JNA fibroblast-induced tubule formation. AZD4547 may have therapeutic potential in the treatment of JNA.

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Management of persistent juvenile angiofibroma after endoscopic resection: Analysis of a single institution series of 74 patients

et al. 2018

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Background Management of persistent juvenile angiofibroma (pJA) after transnasal endoscopic resection is controversial. To better understand its behavior, optimize treatment, and minimize morbidity, we report our experience in pJA focusing on follow‐up strategies and disease progression. Methods A retrospective review of clinical records of all JA cases treated with endoscopic surgery at the Unit of Otorhinolaryngology of the University of Brescia between January 1994 and October 2015 was performed. Results Seventy‐four cases were included. Mean follow‐up was 113 months (6‐266 months). Evolution of pJA was analyzed in 6 cases. Residual lesion size significantly decreased in 3 cases and 2 lesions did not show size variations; significant growth was detected in 1 case of intentional pJA, with diameter increasing by 2.2 mm/yr. Conclusions pJAs may have the tendency to regress spontaneously or remain stable. In selected cases, avoiding treatment of nongrowing pJA in critical areas is a prudent option.

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Current molecular profile of juvenile nasopharyngeal angiofibroma: First comprehensive study from India

Abstract: NA. Laryngoscope, 127:E100-E106, 2017.

Cited by 24 publications

References 38 publications

Biomolecular Analysis of Juvenile Nasopharyngeal Angiofibroma

Biomolecular Analysis of Juvenile Nasopharyngeal Angiofibroma

Inhibition of fibroblast growth factor receptor with AZD4547 mitigates juvenile nasopharyngeal angiofibroma

Management of persistent juvenile angiofibroma after endoscopic resection: Analysis of a single institution series of 74 patients

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