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[Cancer Research 62, 2625-2629, May 1, 2002]
© 2002 American Association for Cancer Research

Regular Articles

Targets of Gene Amplification and Overexpression at 17q in Gastric Cancer1

Asta Varis2, Maija Wolf2, Outi Monni2, Marja-Leena Vakkari, Arto Kokkola, Chris Moskaluk, Henry Frierson, Jr., Steven M. Powell, Sakari Knuutila, Anne Kallioniemi and Wa’el El-Rifai3

Department of Medical Genetics [A. V., M-L. V., S. K.], Biomedicum Biochip Center [O. M.], and Department of Surgery [A. K.], University of Helsinki and Helsinki University Central Hospital, Helsinki 00290, Finland; Cancer Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892 [M. W., O. M., A. K.]; Laboratory of Cancer Genetics, University of Tampere, Tampere 33014, Finland [A. K.]; and Department of Pathology [C. M., H. F.] and Digestive Health Center of Excellence [S. M. P., W. E-R.], University of Virginia Health System, Charlottesville, Virginia 22908-0708

DNA copy number gains and amplifications at 17q are frequent in gastriccancer, yet systematic analyses of the 17q amplicon have not been performed.In this study, we carried out a comprehensive analysis of copy number and expression levels of 636 chromosome 17-specific genes in gastric cancer by using a custom-made chromosome 17-specific cDNA microarray. Analysis of DNA copy number changes by comparative genomic hybridization on cDNA microarray revealed increased copy numbers of 11 known genes (ERBB2, TOP2A, GRB7, ACLY, PIP5K2B, MPRL45, MKP-L, LHX1, MLN51, MLN64, and RPL27) and seven expressed sequence tags (ESTs) that mapped to 17q12-q21 region. To investigate the genes transcribed at the 17q, we performed gene expression analyses on an identical cDNA microarray. Our expression analysis showed overexpression of 8 genes (ERBB2, TOP2A, GRB2, AOC3, AP2B1, KRT14, JUP, and ITGA3) and two ESTs. Of the commonly amplified transcripts, an uncharacterized EST AA552509 and the TOP2A gene were most frequently overexpressed in 82% of the samples. Additional studies will be initiated to understand the possible biological and clinical significance of these genes in gastric cancer development and progression.




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