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[Cancer Research 62, 1256-1260, March 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Clinical Validation of Candidate Genes Associated with Prostate Cancer Progression in the CWR22 Model System using Tissue Microarrays1

Spyro Mousses, Lukas Bubendorf, Urs Wagner, Galen Hostetter, Juha Kononen, Robert Cornelison, Natalie Goldberger, Abdel G. Elkahloun, Niels Willi, Pasi Koivisto, William Ferhle, Mark Raffeld, Guito Sauter and Olli-P Kallioniemi2

Cancer Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892 [S. M., U. W., G. H., J. K., R. C., N. G., A. G. E., O-P. K.]; Institute of Pathology, University of Basel, Basel 4003, Switzerland [L. B., N. W., G. S.]; Laboratory of Cancer Genetics, Tampere University Hospital, 33521 Tampere, Finland [P. K.]; and Department of Pathology, National Cancer Institute, NIH, Bethesda, Maryland 20850 [W. F., M. R.]

To explore molecular mechanisms of prostate cancer progression, we applied tissue microarrays (TMAs) to analyze expression of candidate gene targets discovered by cDNA microarray analysis of the CWR22 xenograft model system. A TMA with 544 clinical specimens from different stages of disease progression was probed by mRNA in situ hybridization and protein immunohistochemistry. There was an excellent correlation (r = 0.96; n = 16) between the expression levels of the genes in the xenografts by cDNA microarray and mRNA in situ hybridization on a TMA. One of the most highly overexpressed genes in hormone-refractory CWR22R xenografts was the S100P gene. This gene, coding for a calcium signaling molecule implicated in the loss of senescence, was also significantly associated with progression in clinical tumors by TMA analysis (P < 0.001), suggesting dysregulation of this pathway in hormone-refractory and metastatic prostate cancers. Conversely, two genes that were down-regulated during tumor progression in the CWR22 model system were validated in vivo: crystallin µ (CRYM) and a LIM-domain protein LMO4 both showed significantly lower mRNA levels in hormone-refractory tumors as compared with primary tumors (P < 0.001). These results illustrate a strategy for rapid clinical validation at the mRNA and protein level of gene targets found to be differentially expressed in cDNA microarray experiments of model systems of cancer.




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