g. gender, age, tumor location, and TNM stage. selleck chem inhibitor All P values 0. 05 were considered as statistically significant. Results The presence of EGFR, KRAS, PIK3CA and PTEN mu tations in Inhibitors,Modulators,Libraries 38 patients were listed in Table 1. Each patient was represented only once, where Inhibitors,Modulators,Libraries for each type of ma terial the information from all the patients samples was merged. An EGFR mutation was identified in 1 of the 38 PSCCE patients, resulting in L858R missense mutation in exon 21. No mutation was found in exons 18,19 and 20. We either did not found KRAS mutations in codons 12, 13 and PIK3CA mutations in exon 9 and exon 20 in all samples. PTEN mutations were detected in 14 out of 38 patients, including exon 5 coding for PTEN missense mutation, exon 6, concur rent exon 5 and exon 6, and exon 8.

No concurrent mutations of these genes were de tected in all samples. Moreover, there were no significant associations between PTEN mutations and clinical patho logic characteristics, e. g. gender, age, tumor location and TNM stage. Discussion China is an endemic Inhibitors,Modulators,Libraries region for esophageal cancers. The incidence has been reported as165 200 100,000 in China, Japan and Eastern Turkey, while it is only 3 100,000 in Europe and USA. Recently many published reports have demonstrated that EGFR mutations were detected in EC cell lines and patients with EC. A phase II study of advanced EC treatment by gefitinib indicated that patients with ESCC had a higher disease control rate. Another phase II trial using gefitinib in advanced EAC showed that gefitinib were an active and gen erally well tolerated treatment for EAC.

However, Inhibitors,Modulators,Libraries whether similar results exist in patients with PSCCE re mains unclear. To date, the mutation status of EGFR and EGFR related genes in patients with PSCCE Inhibitors,Modulators,Libraries have not been reported because of the rare incidence of the specific histological Temsirolimus type of esophageal cancer worldwide. In fact, the reported incidence of PSCCE among all esophageal malignancies is higher in Chinese population than in Caucasians. In this study, we found that only 2. 63% of 38 patients with PSCCE carring EGFR mutations, consistent with data that reported in the previous studies on other histological types of EC, but signifi cantly different from other reports. Possible rea sons for the discrepancy are that ethnic differences in the distribution of the EGFR mutations in EC may exist, and the sensitivity of technique used for mutation detection differs. Furthermore, the only one patient with PSCCE identified for EGFR mutation was L858R missense muta tion in exon 21, termed as gefitinib associated mutations. This suggests the gefitinib based small molecular target therapy possibly can be appropriately applied in treating PSCCE patients that harbor this specific mutation as well.