Abstract

Abstract EGFR and downstream signaling pathway plays important roles in the tumorigenesis in oral squamous cell carcinoma (OSCC). Gene copy number alteration is one the mechanism overexpressing the EGFR protein. We previously demonstrated that EGFR gene amplification was related with lymph node metastasis, tumor invasion and perineural invasion. We appraise the hypothesis that the EGFR gene copy number alteration in the primary tumor can predict that in recurrent tumors or in lymph node metastatic foci. Of 167 primary OSCCs, fluorescence in-situ hybridization (FISH) study showed EGFR polysomy in 19 (11.4%) patients and amplification in 33 (19.8%) patients. EGFR gene amplification was related with lymph node metastasis (χ2 trend test: P = 0.018) Of 57 metastatic lymph nodes, 9 (15.8%) had EGFR polysomy and 14 (24.6%) had EGFR gene amplification. The concordance rate of EGFR gene copy number in primary tumor and lymph node metastasis was 68.4% (McNemar test: P = 0.389). Of 41 recurrent tumors, 5 (12.2%) had EGFR polysomy and 5 (12.2%) had gene amplification. The concordance rate of EGFR gene copy number between primary tumor and recurrence tumor was 65.9% (McNemar test: P = 0.510). From our results, we can predict two-thirds of the EGFR gene copy number alteration in the lymph node metastasis or the recurrent tumor from the analysis of primary tumor. In clinical scenario, for OSCC patients that the lymph nodes or the recurrent tumors are unavailable for EGFR gene copy number analysis, studies from the primary tumors could provide part of the EGFR clonal information in the metastatic or recurrent lesions. Citation Format: Shiang-Fu Huang, Huei-Tzu Chien, Sou-De Cheng, Chun-Ta Liao, Hung-Ming Wang, Ling-Ling Hsieh. EGFR copy number alterations in primary tumors, metastatic lymph nodes and recurrent tumors in areca-quid associated oral squamous cell carcinoma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5026.

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