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Cytogenetics of Prostate Cancer

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Prostate Cancer
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Abstract

The biological behavior of prostate cancer is highly unpredictable. While some patients die with rather than of prostate cancer, others succumb rapidly progressive disease. Although most advanced prostate cancers respond favorably to androgen withdrawal therapy, they eventually recur after a few months or years. There is still no efficient second-line therapy for recurring prostate cancer [29]. There is a need for molecular markers to better predict the biological behavior and guide therapy decisions in individual patients. Altered expression of cancer-related genes is often linked to chromosomal changes. Inactivation of tumor-suppressor genes can be associated with chromosomal deletion, whereas oncogenes are often activated through increased gene copy numbers. Therefore, the identification of chromosomal alterations can be a first step for the identification of previously unknown genes. Different techniques have been used to analyze chromosomal alterations in cancer. Conventional cytogenetic analysis always includes a short-term culturing of tumor cells, which are subsequently arrested in metaphase or prometaphase. After dropping these cells on glass slides, the chromosomes are spread and can be analyzed after Giemsa staining. Major limitations of classical cytogenetics are the need for fresh tissue and the risk of selecting non-representative clones (neoplastic or non-neoplastic) during cell culture. The simultaneous analysis of the entire genome and the ability to detect structural changes (translocations, inversions) are the strongest advantages of cytogenetics, which has recently been further improved by the ability to simultaneousy identify all chromosomes in different colors [69].

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Bubendorf, L. (2003). Cytogenetics of Prostate Cancer. In: Hofmann, R., Heidenreich, A., Moul, J.W. (eds) Prostate Cancer. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56321-8_2

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  • DOI: https://doi.org/10.1007/978-3-642-56321-8_2

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