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Open Access Research

Lack of EGFR mutations benefiting gefitinib treatment in adenocarcinoma of esophagogastric junction

Wen-Ping Wang, Kang-Ning Wang, Qiang Gao and Long-Qi Chen*

Author Affiliations

Department of Thoracic Surgery, West China Hospital, Sichuan University, Chengdu 610041, China

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World Journal of Surgical Oncology 2012, 10:14  doi:10.1186/1477-7819-10-14

Published: 17 January 2012



The epidermal growth factor receptor (EGFR) inhibitor, gefitinib, has been reported to successfully treat advanced non-small cell lung cancer patients with genetic mutations in EGFR. The aim of this study was to investigate the existence of EGFR mutations in carcinoma of esophagogastric junction, and also to explore the possibility of treating carcinoma of esophagogastric junction using gefitinib.


From Aug. 2009 to Jun. 2010, 65 patients with carcinoma of esophagogastric junction underwent surgical resection. The tumor tissue and corresponding blood specimens were collected from all cases. The DNA was extracted and PCR amplification was accomplished based on designed primers for exons 18, 19, 20, and 21. EGFR exons 18, 19, 20 and 21 of both cancer cell and white blood cell were finally successfully sequenced.


In exon 20, a variant from CAG to CAA at codon 787 (2361G-> A) was identified in 19 patients, which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells. This EGFR alteration was a synonymous single nucleotide polymorphism (SNP) since CAA and CAG were encoding the same amino-acid of Glutamine (Q787Q, NCBI database 162093G > A, SNP ID: rs10251977). No genetic alteration was found in exons 18, 19 or 21.


Adenocarcinoma of esophagogastric junction rarely presents EGFR mutation, especially gefitinib-associated mutations such as L858R, or delE746-A750. This means that the gefitinib-based gene target therapy should not be recommended for treating carcinoma of esophagogastric junction.

Epidermal growth factor receptor; Adenocarcinoma of esophagogastric junction; Gene mutation; Single nucleotide polymorphism; Gefitinib