Abstract
Both, analysis of copy number variations (CNV) and gene expression profiling allow the identification of pathological mechanism associated with tumor development and progression. The aim of the study was to combine the two technologies to analyse a potential correlation of gene expression and chromosomal changes in colon cancer and to identify regions with potential clinical impact. Gene expression and single nucleotide polymorphism were collected from 32 stage UICC II colon cancer patients after tumor cell enrichment by macrodissection (Human Genome U133 Plus 2.0 Array and Human Mapping 500K Set). Among several observed alterations we could show that chromosomal region 13q31.3, comprising mikro-RNA Cluster 17–92 (C13orf25), is gained in 22/32 (69 %) of all cancer samples (CNV(Med) 2,4). Comparison of CNV and differential gene expression in this region shows an overexpression of C13orf25 in cancer tissue of 17/ 32 samples (foldchange (T vs. N) > 1,5). Patients with an amplification of 13q31.3 showed an overexpression of C13orf25 in 15 out of 22 patients (Foldchange (T vs. N) = 1,9) compared to samples with normal copy number and no overexpression of C13orf25. Known chromosomal amplification and overexpression of members of the MYC-dependant microRNA cluster 17–92 (miR-17–92) in cancer tissues could be demonstrated in colon cancer. Chromosomal amplification and synchronous relative overexpression of miR-17–92 may be a hint for a correlation of CNV and differential gene expression. Our strategy of combining both technologies allows the identification of molecular alterations with potential clinical impact in colon cancer.
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© 2008 Springer Medizin Verlag Heidelberg
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Gröne, J., Buhr, H.J., Hummel, M., Lenze, D. (2008). Microarray-basierte Analysen der genomischen Kopienzahl und der Genexpression beim Kolonkarzinom. In: Arbogast, R., Schackert, H.K., Bauer, H. (eds) Chirurgisches Forum 2008. Deutsche Gesellschaft für Chirurgie, vol 37. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-78833-1_7
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DOI: https://doi.org/10.1007/978-3-540-78833-1_7
Publisher Name: Springer, Berlin, Heidelberg
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