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

Wang WP, Wang KN, Gao Q, Chen LQ - World J Surg Oncol (2012)

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

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

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

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Related in: MedlinePlus

The variant from CAG to CAA at codon 787 in exon 20. The variant from CAG to CAA at codon 787 in exon 20 (arrows), which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells, and this was a synonymous mutation because CAA and CAG were encoding the same amino-acid of Glutamine (Q787Q).
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Figure 1: The variant from CAG to CAA at codon 787 in exon 20. The variant from CAG to CAA at codon 787 in exon 20 (arrows), which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells, and this was a synonymous mutation because CAA and CAG were encoding the same amino-acid of Glutamine (Q787Q).

Mentions: The DNA sequencing of exons 18, 19, 20 and 21 was successfully performed and output with the *. ABL format file by Chromas 2.0. We analyzed all the DNA sequences. In exon 20, a variant from CAG to CAA at codon 787 (2361G-> A) was identified in 19 patients (29.2%) (Figure 1), which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells. No other variants were discovered in exons 18, 19, or 21. The discovered EGFR variant in exon 20 was a synonymous mutation because CAA and CAG were encoding the same amino-acid of Glutamine (Q787Q). It was considered as single nucleotide polymorphism (SNP). This SNP has been deposited in NCBI database (162093G > A, SNP ID: rs10251977).


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

Wang WP, Wang KN, Gao Q, Chen LQ - World J Surg Oncol (2012)

The variant from CAG to CAA at codon 787 in exon 20. The variant from CAG to CAA at codon 787 in exon 20 (arrows), which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells, and this was a synonymous mutation because CAA and CAG were encoding the same amino-acid of Glutamine (Q787Q).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3278359&req=5

Figure 1: The variant from CAG to CAA at codon 787 in exon 20. The variant from CAG to CAA at codon 787 in exon 20 (arrows), which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells, and this was a synonymous mutation because CAA and CAG were encoding the same amino-acid of Glutamine (Q787Q).
Mentions: The DNA sequencing of exons 18, 19, 20 and 21 was successfully performed and output with the *. ABL format file by Chromas 2.0. We analyzed all the DNA sequences. In exon 20, a variant from CAG to CAA at codon 787 (2361G-> A) was identified in 19 patients (29.2%) (Figure 1), which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells. No other variants were discovered in exons 18, 19, or 21. The discovered EGFR variant in exon 20 was a synonymous mutation because CAA and CAG were encoding the same amino-acid of Glutamine (Q787Q). It was considered as single nucleotide polymorphism (SNP). This SNP has been deposited in NCBI database (162093G > A, SNP ID: rs10251977).

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

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

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Show MeSH
Related in: MedlinePlus