Genetic alterations in Ki-ras and Ha-ras genes in Juvenile Nasopharyngeal Angiofibromas and head and neck cancer

Abstract

Our results demonstrate for the first time that mutations of Ki-ras and Ha-ras genes are not associated with the development of JNA and confirm previous reports indicating that activating ras mutations are absent or rarely involved in head and neck tumors from western world patients. Furthermore, our findings suggest that overexpression of Ha-ras, rather than mutations, might be an important factor in the development and progression of head and neck tumors.

H-Ras mutation modulates the expression of major cell cycle regulatory proteins and disease prognosis in oral carcinoma

“…Similar to the present study, Ras overexpression was reported to be associated with favourable prognosis in HNSCC, 34 although, conflicting reports are also available. 35 In summary, the present study demonstrated that H-Ras mutation associated with expression of key cell cycle regulatory proteins such as cyclin D1, CDK4, Rb and p16 in vivo. It seems that molecular phenotype associated with mutant Ras guard against the oncogenic potential of H-Ras mutation in oral carcinoma and thus provide favourable prognosis to the patients.…”

Differential expression of Epstein-Barr virus-encoded RNA and several tumor-related genes in various types of nasopharyngeal epithelial lesions and nasopharyngeal carcinoma using tissue microarray analysis

“…NPC has been reported to be strongly associated with the Epstein-Barr virus (EBV) [6,9,10,13,14]. In addition, growing evidences demonstrate that alterations of some oncogenes and tumor suppressor genes are important factors in the multistep process of nasopharyngeal carcinogenesis [9,[13][14][15][16][17][18][19][20][21]. The p53 gene, a well-known tumor suppressor gene, is rarely mutated in NPC.…”

“…However, high expression of p53 protein revealed by immunohistochemistry (IHC) in primary tumors suggests that abnormal p53 stabilization plays a key role in NPC, particularly in the nasopharyngeal epithelium with EBV infection [6,15,17]. Members of the ras gene family are structurally related and code for a protein (p21) known to play an important role in the regulation of normal signal transduction and cell growth [21,22]. Ras oncogene protein (p21) can induce the transformation of human solid tumors [22].…”

“…Ras oncogene protein (p21) can induce the transformation of human solid tumors [22]. Overexpression of Ha-ras, rather than mutations, may be an important factor in the development and progression of head and neck tumors [21]. The bcl-2 oncogene inhibits apoptosis and implicates in both differentiation of normal keratinocyte and pathogenesis of epithelial malignancy [18,23].…”

Biomolecular Analysis of Juvenile Nasopharyngeal Angiofibroma

“…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.…”