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Molecular portrait of human kidney carcinomas: The cDNA microarray profiling of kinases and phosphatases involved in the cell signaling control

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons77854

Cheburkin,  Y. V.
Ullrich, Axel / Molecular Biology, Max Planck Institute of Biochemistry, Max Planck Society;
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78237

Knyazeva,  T. G.
Ullrich, Axel / Molecular Biology, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78812

Ullrich,  A.
Ullrich, Axel / Molecular Biology, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78238

Knyazev,  P. G.
Ullrich, Axel / Molecular Biology, Max Planck Institute of Biochemistry, Max Planck Society;

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Citation

Cheburkin, Y. V., Knyazeva, T. G., Peter, S., Knyazev, Y. P., Karelin, M. I., Shkolnik, M. I., et al. (2002). Molecular portrait of human kidney carcinomas: The cDNA microarray profiling of kinases and phosphatases involved in the cell signaling control. Molecular Biology, 36(3), 376-384.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-6F42-1
Abstract
Hybridization with cDNA arrays was used to obtain expression profiles of 214 protein-tyrosine kinase, protein-tyrosine phosphatase, dual specificity phosphatase, and other genes for kidney carcinomas (KC) and normal kidney tissues of 34 patients and for seven carcinoma cell lines. Computer analysis revealed three clusters of genes coexpressed in KC. The proliferating- cell gene cluster included MET, VIM, MYC, TOM, PCNA. The neoangiogenesis and blood-cell gene cluster included LCK, HCK, FGR, MAIM, CSFR1, VEGF, FLT1, and KDR. The cluster corresponding to normal, differentiated kidney cells included ERBB2 (HER2) for receptor protein-tyrosine kinase, several phosphatase genes (PTPRE, PTPRB, DUSP9), and EGF. The results suggested that MET, DUSP9, PCNA, TOM, and VIM may serve as diagnostic and prognostic markers in KC. Tubulin and topoisomerase II were assumed to be promising targets for cell proliferation inhibitors in KC.