© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 20, 1758-1764,
October 20, 1999
© 1999 Oxford University Press
REPORTS |
Hormone Therapy Failure in Human Prostate Cancer: Analysis by Complementary DNA and Tissue Microarrays
Affiliations of authors: L. Bubendorf, M. Kolmer, J. Kononen, S. Mousses, Y. Chen, O.-P. Kallioniemi, Cancer Genetics Branch, National Human Genome Research Institute, Bethesda, MD; P. Koivisto, E. Mahlamäki, Laboratory of Cancer Genetics, Tampere University Hospital, Finland; P. Schraml, H. Moch, N. Willi, M. J. Mihatsch, G. Sauter (Institute of Pathology), T. C. Gasser (Urologic Clinics), University of Basel, Switzerland; A. G. Elkahloun, Research Genetics, Inc., Huntsville, AL; T. G. Pretlow, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Present address: M. Kolmer, National Public Health Institute, Department of Human Molecular Genetics, Helsinki, Finland.
Correspondence to: Olli-P. Kallioniemi, M.D., Ph.D., National Institutes of Health, 49 Convent Dr., MSC 4470, Rm. 4A24, Bethesda, MD 20892-4470 (e-mail: okalli{at}nhgri.nih.gov).
BACKGROUND: The molecular mechanisms underlying the progression of prostate cancer during hormonal therapy have remained poorly understood. In this study, we developed a new strategy for the identification of differentially expressed genes in hormone-refractory human prostate cancer by use of a combination of complementary DNA (cDNA) and tissue microarray technologies. METHODS: Differences in gene expression between hormone-refractory CWR22R prostate cancer xenografts (human prostate cancer transplanted into nude mice) and a xenograft of the parental, hormone-sensitive CWR22 strain were analyzed by use of cDNA microarray technology. To validate the data from cDNA microarrays on clinical prostate cancer specimens, a tissue microarray of specimens from 26 prostates with benign prostatic hyperplasia, 208 primary prostate cancers, and 30 hormone-refractory local recurrences was constructed and used for immunohistochemical detection of protein expression. RESULTS: Among 5184 genes surveyed with cDNA microarray technology, expression of 37 (0.7%) was increased more than twofold in the hormone-refractory CWR22R xenografts compared with the CWR22 xenograft; expression of 135 (2.6%) genes was reduced by more than 50%. The genes encoding insulin-like growth factor-binding protein 2 (IGFBP2) and 27-kd heat-shock protein (HSP27) were among the most consistently overexpressed genes in the CWR22R tumors. Immunohistochemical analysis of tissue microarrays demonstrated high expression of IGFBP2 protein in 100% of the hormone-refractory clinical tumors, in 36% of the primary tumors, and in 0% of the benign prostatic specimens (two-sided P = .0001). Overexpression of HSP27 protein was demonstrated in 31% of the hormone-refractory tumors, in 5% of the primary tumors, and in 0% of the benign prostatic specimens (two-sided P = .0001). CONCLUSIONS: The combination of cDNA and tissue microarray technologies enables rapid identification of genes associated with progression of prostate cancer to the hormone-refractory state and may facilitate analysis of the role of the encoded gene products in the pathogenesis of human prostate cancer.
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