Biomolecular Analysis of Juvenile Nasopharyngeal Angiofibroma

Juvenile nasopharyngeal angiofibroma (JNA), a rare type of tumor that occurs most frequently in adolescent males, is difficult to treat. The relationship between JNA and certain biomolecules has been the subject of a great deal of research conducted over a long period. This review summarizes the research on the etiopathogenesis of JNA. 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 [2,5–7,9–13,15–17,25,27,28,32– 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. Among these, GSTM1-null genotype gene seems important. Expression of GSTM1 mRNA (which encodes glutathione S-transferase M1, a protein involved in detoxification) should be normally in all human beings. When this is not expressed there is an increased risk of developing some malignancies [17,42]. Two studies performed on GSTM1-null genotype [17,33]. In both studies, the GSTM1-null genotype was associated with the formation of JNA. Discussion Some authors have suggested that cellular structural proteins are involved in the etiopathogenesis of JNA. For example, E-cadherin, N-cadherin, α-catenin, β-catenin, γ-catenin, bone morphogenic protein 4 (BMP4), MNF116, CAM5.2, desmin, vimentin, calponin [2,13,14,30,31,41] have all been studied, and both β-catenin [2,14,30,31,41] and vimentin [13] were shown to be associated with JNA. 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 [6,8,12,13,16,36–38]. 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. There have also been investigations regarding the associations between biomolecules and the prognosis of JNA, with ER, MMP-9, and IL-17 all being shown to be associated with poor prognosis [23,37,38]. Carlos et al. postulated that human herpes virus-8 (HHV-8) and Epstein-Barr virus (EBV) may play roles in the etiology of JNA, but their results indicated no such associations of these viruses with the pathogenesis of JNA [4]. Citation: Mazlumoglu MR (2017) Biomolecular Analysis of Juvenile Nasopharyngeal Angiofibroma. J Mol Genet Med 11: 304 doi:10.4172/17470862.1000304 Volume 11 • Issue 4 • 1000304 J Mol Genet Med, an open access journal ISSN: 1747-0862 Page 2 of 3


Introduction
Juvenile nasopharyngeal angiofibroma (JNA) is a benign tumor of the nasopharynx, which accounts for 0.5% of all head and neck tumors. Although it can occur in all age groups, it is most common in adolescents and young adults between 14 and 25 years of age. It is also more common in males than in females [1].
Although JNA is histologically benign, it shows locally invasive behavior and is treated surgically. However, recurrence rates are high, at up to 42% [2]. The most common complication of surgery is bleeding. Therefore, studies on JNA have focused on the difficulty of surgical treatment and high relapse rate. Primary or adjuvant therapy targeting biomolecules secreted from tumor tissue in large quantities (molecular-targeted therapy) can help to reduce the rates of complications, can be used primarily in the treatment, can render otherwise inoperative tumors amenable to surgical intervention, and can be used in palliative treatment.

Literature Review
The pathogenesis of JNA is still unknown. There have been a number of studies regarding tumor formation and growth in JNA, and regarding its prognostic. These studies took into consideration the male predominance of the tumor, its vascular nature, and its common onset in adolescence. The roles of growth factors, hormone receptors, tumor suppressor genes, oncogenes, and cytokines in the etiopathogenesis of JNA have all been evaluated (Table 1)  .
There have also been investigations regarding the associations between biomolecules and the prognosis of JNA, with ER, MMP-9, and IL-17 all being shown to be associated with poor prognosis [23,37,38].

Carlos et al. postulated that human herpes virus-8 (HHV-8) and
Epstein-Barr virus (EBV) may play roles in the etiology of JNA, but their results indicated no such associations of these viruses with the pathogenesis of JNA [4].

Conclusion
A number of studies have indicated associations between certain biomolecules and JNA. However, molecular targeting has not yet been applied during clinical treatment. Nevertheless, these studies are promising in terms of the future development of possible alternative methods to surgical treatment. Also, the studies about JNA were summarized in this review. These studies were presented in the form of a table. This presentation can help authors who plan to study on JNA. Ponti et al. [14] β--catenin, E-cadherin, AR, VEGFR-2 β--catenin, VEGFR-2