OBJECTIVES: Chromosomal instability is hallmark of carcinoma. Amplification of chromosome 17q11-q12 is present in some oral squamous cell cancer (OSCC) cases. In this study, we investigated the copy number variations of ERBB2 gene, which is located at this locus in collected OSCC samples and their correlation with tumor progression and gene expression. STUDY DESIGN: Quantitative real-time polymerase chain reaction was performed to detect the copy number of ERBB2 gene and the mRNA expression in 92 OSCC samples with matched adjacent normal tissues (ANTs). Proportional odds regression and 2-way repeated measurement analysis of variance were used to analyze the association between copy number variations and mRNA expression of the targeted gene. RESULTS: Copy number gains of ERBB2 were detected in some of the OSCCs (19.6%, 18/92) and correlated with tumor stage (P < .001). Copy number gains of ERBB2 also showed a positive correlation with mRNA overexpression in OSCCs (P < .001). However, enhanced ERBB2 mRNA expression was also detected in a group of OSCC samples with unaltered copy number of ERBB2 gene (P < .05). CONCLUSIONS: Copy number increase of ERBB2 is observed in OSCCs and correlates with gene overexpression in these tumors. In addition, overexpression of ERBB2 is also observed in some OSCCs that lack copy number changes, indicating involvement of another mechanism.
OBJECTIVES: Chromosomal instability is hallmark of carcinoma. Amplification of chromosome 17q11-q12 is present in some oral squamous cell cancer (OSCC) cases. In this study, we investigated the copy number variations of ERBB2 gene, which is located at this locus in collected OSCC samples and their correlation with tumor progression and gene expression. STUDY DESIGN: Quantitative real-time polymerase chain reaction was performed to detect the copy number of ERBB2 gene and the mRNA expression in 92 OSCC samples with matched adjacent normal tissues (ANTs). Proportional odds regression and 2-way repeated measurement analysis of variance were used to analyze the association between copy number variations and mRNA expression of the targeted gene. RESULTS: Copy number gains of ERBB2 were detected in some of the OSCCs (19.6%, 18/92) and correlated with tumor stage (P < .001). Copy number gains of ERBB2 also showed a positive correlation with mRNA overexpression in OSCCs (P < .001). However, enhanced ERBB2 mRNA expression was also detected in a group of OSCC samples with unaltered copy number of ERBB2 gene (P < .05). CONCLUSIONS: Copy number increase of ERBB2 is observed in OSCCs and correlates with gene overexpression in these tumors. In addition, overexpression of ERBB2 is also observed in some OSCCs that lack copy number changes, indicating involvement of another mechanism.