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[Cancer Research 59, 803-806, February 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 803-806, February 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Survey of Gene Amplifications during Prostate Cancer Progression by High-Throughput Fluorescence in Situ Hybridization on Tissue Microarrays1

Lukas Bubendorf, Juha Kononen, Pasi Koivisto, Peter Schraml, Holger Moch, Thomas C. Gasser, Niels Willi, Michael J. Mihatsch, Guido Sauter and Olli-P. Kallioniemi2

Laboratory of Cancer Genetics, National Human Genome Research Institute, NIH [L. B., J. K., O-P. K.], Bethesda, Maryland 20892-4470; Laboratory of Cancer Genetics, Tampere University Hospital, 33521 Tampere, Finland [P. K.]; and Institute for Pathology [P. S., H. M., N. W., M. J. M., G. S.] and Urologic Clinics [T. C. G.], University of Basel, CH-4003 Basel, Switzerland

Prostate cancer development and progression is driven by the accumulation of genetic changes, the nature of which remains incompletely understood. To facilitate high-throughput analysis of molecular events taking place in primary, recurrent, and metastatic prostate cancer, we constructed a tissue microarray containing small 0.6-mm cylindrical samples acquired from 371 formalin-fixed blocks, including benign prostatic hyperplasia (n = 32) and primary tumors (n = 223), as well as both locally recurrent tumors (n = 54) and metastases (n = 62) from patients with hormone-refractory disease. Fluorescence in situ hybridization (FISH) was applied to the analysis of consecutive tissue microarray sections with probes for five different genes. High-level (>=3X) amplifications were very rare (<2%) in primary prostate cancers. However, in metastases from patients with hormone-refractory disease, amplification of the androgen receptor gene was seen in 22%, MYC in 11%, and Cyclin-D1 in 5% of the cases. In specimens from locally recurrent tumors, the corresponding percentages were 23, 4, and 8%. ERBB2 and NMYC amplifications were never detected at any stage of prostate cancer progression. In conclusion, FISH to tissue microarray sections enables high-throughput analysis of genetic alterations contributing to cancer development and progression. Our results implicate a role for amplification of androgen receptor in hormonal therapy failure and that of MYC in the metastatic progression of human prostate cancer.




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J. Richter, U. Wagner, J. Kononen, A. Fijan, J. Bruderer, U. Schmid, D. Ackermann, R. Maurer, G. Alund, H. Knonagel, et al.
High-Throughput Tissue Microarray Analysis of Cyclin E Gene Amplification and Overexpression in Urinary Bladder Cancer
Am. J. Pathol., September 1, 2000; 157(3): 787 - 794.
[Abstract] [Full Text] [PDF]

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M. Drobnjak, I. Osman, H. I. Scher, M. Fazzari, and C. Cordon-Cardo
Overexpression of Cyclin D1 Is Associated with Metastatic Prostate Cancer to Bone
Clin. Cancer Res., May 1, 2000; 6(5): 1891 - 1895.
[Abstract] [Full Text]

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A. K. Walch, H. F. Zitzelsberger, J. Bruch, G. Keller, D. Angermeier, M. M. Aubele, J. Mueller, H. Stein, H. Braselmann, J. R. Siewert, et al.
Chromosomal Imbalances in Barrett’s Adenocarcinoma and the Metaplasia-Dysplasia-Carcinoma Sequence
Am. J. Pathol., February 1, 2000; 156(2): 555 - 566.
[Abstract] [Full Text] [PDF]

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P. Schraml, J. Kononen, L. Bubendorf, H. Moch, H. Bissig, A. Nocito, M. J. Mihatsch, O.-P. Kallioniemi, and G. Sauter
Tissue Microarrays for Gene Amplification Surveys in Many Different Tumor Types
Clin. Cancer Res., August 1, 1999; 5(8): 1966 - 1975.
[Abstract] [Full Text] [PDF]

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A. Dellas, J. Torhorst, F. Jiang, J. Proffitt, E. Schultheiss, W. Holzgreve, G. Sauter, M. J. Mihatsch, and H. Moch
Prognostic Value of Genomic Alterations in Invasive Cervical Squamous Cell Carcinoma of Clinical Stage IB Detected by Comparative Genomic Hybridization
Cancer Res., July 1, 1999; 59(14): 3475 - 3479.
[Abstract] [Full Text] [PDF]


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