Esophageal carcinoma cell line with high EGFR polysomy is responsive to gefitinib.

[esophageal adenocarcinoma]

It has previously been shown that gefitinib-treated patients with epidermal growth factor receptor (EGFR ) gene amplification or high polysomy had a statistically significant improvement in response , time to progression , and survival in non-small cell lung cancer (NSCLC ). Only few studies utilizing anti-EGFR treatment in advanced esophageal adenocarcinomas have been performed and the results have been heterogeneous . The aim of this study was to evaluate EGFR -targeted therapy with gefitinib in esophageal adenocarcinoma with a high EGFR polysomy .Novel esophageal cell lines PT 6216 and LN 6216 c were established from primary tumor and lymph node metastasis of a patient with highly aggressive and metastatic adenocarcinoma . Pathological examination including tumor differentiation and prognostic marker analysis , immunohistochemical EGFR expression analysis , EGFR fluorescence in situ hybridization , and mutation analysis were performed . Response of novel cell lines to gefitinib treatment was evaluated by cell proliferation and vitality assays . Fifty -four esophageal adenocarcinoma specimens were evaluated for EGFR gene copy gain .The primary tumor cell line PT 6216 and the lymph node cell line LN 6216 c show a homogenously high polysomy for EGFR determined by FISH analysis . Cell proliferation and vitality are highly sensitive to the tyrosine kinase inhibitor gefitinib compared to esophageal control cells without a high polysomy for EGFR . High polysomy for EGFR was found in 35 % of patients .We show for the first time a significant treatment response to the EGFR tyrosine kinase inhibitor gefitinib in esophageal tumor cells with a high polysomy for EGFR , suggesting a future role of anti-EGFR therapy for esophageal adenocarcinoma patients with a high EGFR polysomy .