Abstract
BackgroundThe epidermal growth factor receptor (EGFR) is an available target of effective anti-EGFR therapy for human breast cancer. The aim of this study was to assess the presence of EGFR gene amplification and mutations in breast cancer and to analyze the association between the statuses of these two gene alterations.Materials and methodsEGFR gene amplification and mutations were investigated in formalin-fixed, paraffin-embedded tissues from 139 Chinese female patients with breast cancer by means of fluorescence in-situ hybridization (FISH) and fluorescently labeled real-time quantitative polymerase chain reaction (RT-PCR), respectively.ResultsEGFR gene amplification was observed in 46/139 (33.1%) of cases by FISH. Based on RT-PCR, 2/139 (1.4%) samples had EGFR gene mutations. Overall, only 1 (0.7%) of the cases was identified with both whole gene amplification and mutation, and 92 (66.2%) of cases were negative for both. High gene copy numbers of EGFR had significant correlation with the occurrence of EGFR protein expressions (P = 0.002).ConclusionIn this study, EGFR mutations were presented in only two samples, indicating that EGFR mutations should not be employed in future trials with anti-EGFR therapies for breast cancer. However, EGFR whole gene amplification is frequently observed in patients with breast cancer. It will be of significant interest to investigate whether EGFR gene copy number is a suitable screening test for EGFR-targeted therapy for breast cancer.
Highlights
The human epidermal growth factor receptor (HER/ EGFR/ErbB) family of receptor tyrosine kinases is comprised of four transmembrane growth factor receptor proteins that share similarities in structure and function
Due to the biologic significance of EGFR molecular signaling in carcinomas, several monoclonal antibodies against the ligand-binding domain of EGFR and small molecule tyrosine kinase inhibitors of the tyrosine kinase domain of EGFR have been investigated in the therapy of malignant tumors [9,10,11,12,13,14,15,16]
Our results showed that there was no correlation between EGFR and human epidermal growth factor receptor-2 (HER2) protein expression (P = 0.567), which might indicated that activated EGFR can form heterodimer with HER2, and with other members of ErbB family
Summary
The human epidermal growth factor receptor (HER/ EGFR/ErbB) family of receptor tyrosine kinases is comprised of four transmembrane growth factor receptor proteins that share similarities in structure and function. EGFR is a 170 kDa transmembrane protein consisting of an intracellular domain (tyrosine kinase domain), a short phosphatidyl inositol 3’ kinase (PI3K) and Akt pathway and Ras/MAPK pathway are major signaling mechanisms, and they function in the control of several important biologic processes, including cell proliferation, survival, angiogenesis, and migration as well as resistance to apoptosis [6,7,8]. It is important to study whether EGFR is overexpressed in patients with breast cancer since these patients can be given specific EGFR molecule tyrosine kinase inhibitors such as gefitinib and lapatinib [15,16]. The epidermal growth factor receptor (EGFR) is an available target of effective anti-EGFR therapy for human breast cancer. The aim of this study was to assess the presence of EGFR gene amplification and mutations in breast cancer and to analyze the association between the statuses of these two gene alterations
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