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From the Cancer Genetics Branch,*National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland; Department of Haematology,
Cancercytogenetics Laboratory, Aarhus University Hospital, Aarhus, Denmark; the Biomedicum Biochip Center,
Biomedicum Helsinki, Helsinki, Finland; the Laboratory of Cancer Genetics,¶the Institute of Medical Technology, University of Tampere and Tampere University Hospital, Tampere, Finland; and the Institute of Pathology,
University of Basel, Basel, Switzerland
The chromosomal region 17q23 has been shown to be commonly amplified in breast tumors, especially those with poor prognosis. In addition to breast cancer, studies by comparative genomic hybridization have implicated the involvement of 17q23 in other tumor types as well. Here we performed a large-scale survey on the distribution and frequency of the 17q23 copy number increases across different tumor types using fluorescence in situ hybridization on tissue microarrays containing 4788 specimens. A total of 4429 tumor samples representing 166 different tumor categories and 359 normal tissue samples from 40 different tissue categories were analyzed. Successful hybridizations were observed in 3520 of the 4788 specimens (74%). Increased 17q23 copy number was detected in 15% of the evaluable specimens with tumors originating from the lung, mammary gland, and soft tissue being most frequently affected. Interestingly, high-level amplification was detected only in 2% of the tumors and was generally restricted to mammary tumors. In addition, we observed an association between the frequency of increased 17q23 copy number and tumor progression in various tumor types. These results indicate that increased 17q23 copy number occurs frequently in several different tumor types suggesting that increased dosage of genes in this region might play a role in development and progression of many tumor types.
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