Genome‐wide profiling of oral squamous cell carcinoma

• DOI: 10.1002/path.1640
• Publication Date: 2004-09-16T12:02:30Z
• Authors: Yann‐Jang Chen; Shu‐Chun Lin; Tsai Kao; Che‐Shoa Chang; Pei‐She Hong; Tzong‐Ming Shieh; Kuo‐Wei Chang
• Keywords: Caspase 8; Fibroblast Growth Factor 3; Fibroblast Growth Factor 4; Genes, myc; Nucleic Acid Hybridization; DNA, Neoplasm; Middle Aged; Immunohistochemistry; Neoplasm Proteins; Fibroblast Growth Factors; 03 medical and health sciences; 0302 clinical medicine; Caspases; Lymphatic Metastasis; Proto-Oncogene Proteins; Plasminogen Activator Inhibitor 1; Carcinoma, Squamous Cell; Cluster Analysis; Humans; Mouth Neoplasms; RNA, Messenger; Oligonucleotide Array Sequence Analysis

AbstractOral squamous cell carcinoma (OSCC) is a common malignancy, the incidence of which is particularly high in some Asian countries due to the geographically linked areca quid (AQ) chewing habit. In this study, array‐based comparative genomic hybridization was used to screen microdissected OSCCs for genome‐wide alterations. The highest frequencies of gene gain were detected for TP63, Serpine1, FGF4/FGF3, c‐Myc and DMD. The highest frequencies of deletion were detected for Caspase8 and MTAP. Gained genes, classified by hierarchical clustering, were mainly on 17q21–tel; 20q; 11q13; 3q27–29 and the X chromosome. Among these, gains of EGFR at 7p, FGF4/FGF3, CCND1 and EMS1 at 11q13, and AIB1 at 20q were significantly associated with lymph node metastasis. The genomic profiles of FHIT and EXT1 in AQ‐associated and non‐AQ‐associated OSCCs exhibited the most prominent differences. RT‐PCR confirmed the significant increase of TP63 and Serpine1 mRNA expression in OSCC relative to non‐malignant matched tissue. A significant increase in Serpine1 immunoreactivity was observed from non‐malignant matched tissue to OSCC. However, there was no correlation between the frequent genomic loss of Caspase 8 and a significant decrease in Caspase8 expression. These data demonstrate that genomic profiling can be useful in analysing pathogenetic events involved in the genesis or progression of OSCC. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.