[Molecular pathology of prostate carcinoma. Academic playground or guide for diagnosis and therapy planning?].
No effective therapy exists for late-stage hormone-refractory prostate cancer. It would therefore be important to better understand the biological basis of prostate cancer progression. Since cancer is based on genetic alterations, detection of chromosomal changes can pinpoint critical genes and highlight mechanisms of cancer development and progression. Studies by comparative genomic hybridization (CGH) identified recurrent chromosomal aberrations across the progression from organ-confined to late-stage hormonerefractory cancer. These include frequent losses at 8p, 6q, 13q and 18q suggesting relevant tumor-suppressor genes on these chromosomal arms. In contrast, several genes with oncogenic function are likely to reside on 8 q, which is frequently gained in advance stages. Importantly, there are several high-level amplifications in hormone-refractory and metastatic prostate cancers including Xq11-12, 1q21-25, 8q21, 8q24, and 10q22 that may pinpoint to potent oncogenes. The high-level amplification of the androgene receptor at Xq11-12 is a paradigm as to how molecular cytogenetics can elucidate the molecular mechanisms of hormone-refractory growth. Target gene identification of amplifications may lead to new diagnostic tools and therapies of advanced prostate cancer.
Bubendorf
L
L
Institut für Pathologie, Universitätsspital Basel, Basel, Schweiz. lbubendorf@uhbs.ch
D002869:Chromosome Aberrations; D002874:Chromosome Mapping; D002887:Chromosomes, Human, Pair 18; D002896:Chromosomes, Human, Pair 6; D002898:Chromosomes, Human, Pair 8; D018450:Disease Progression; D006801:Humans; D008297:Male; D009362:Neoplasm Metastasis; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology* / Q000628:therapy