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Somatic Molecular Genetics of Prostate Cancer

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Male Reproductive Cancers

Part of the book series: Cancer Genetics ((CANGENETICS))

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Abstract

Despite progress in diagnosis and treatment, prostate cancer is still one of the most frequent lethal diseases in men in Western countries. Today, an increasing number of prostate cancers are detected through elevated serum prostate-specific antigen (PSA) levels. PSA detection is very sensitive. Determining free versus total PSA serum level has enabled the achievement of better specificity (Balk et al. 2003), however, this tool remains imperfect. Many patients undergo unnecessary diagnostic procedures, experiencing physiological and psychological stress. Similarly, current techniques such as imaging and biopsies are not optimal thus, hopes are high for the discovery of new molecular markers for prostate cancer. Studying prostate cancer progression may reveal new insights into the molecular mechanisms of cancer development to help improve prevention, provide better tools for diagnosis, as well as for prognosis and treatment.

There is no site-specific inherited prostate cancer susceptibility gene, but epidemiological studies have demonstrated familial clustering of prostate cancer suggesting an important role of hereditary factors in the development of the disease. Almost 25% of all prostate cancer occurs in family clusters and about 9% can be attributed to hereditary prostate cancer with an autosomal dominant transmission (Carter et al. 1993; Gronberg et al. 1997; Schaid et al. 1998; Langeberg et al. 2007). Men having an affected first-degree relative have two- to threefold higher risk of developing prostate cancer compared with men with no family history (Johns and Houlston 2003). Studies of twins showed higher frequency for prostate cancer in monozygotic as compared to dizygotic twins (Lichtenstein et al. 2000). Several chromosomes may harbor high-penetrance prostate cancer susceptibility genes. Molecular studies have identified three candidate susceptibility genes: the HPC2/ELAC2 gene located at 17p12 encoding a protein with a poorly defined function (Tavtigian et al. 2001), the putative tumor suppressor gene RNASEL located at 1q24–q25 (Carpten et al. 2002), and the MSR1 gene located at 8p22–23 (Xu et al. 2002). However, no functional study has clearly shown that they have a clear role as ­susceptibility genes and thus further investigations are needed. These issues are discussed in detail in the chapters of Lange, and Eeles and colleagues.

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Acknowledgments

Laure Humbert received studentships from the McGill Urology Division and from the Research Institute of the McGill University Health Centre. The work from Mario Chevrette’s laboratory (CD9 section) was funded by the Cancer Research Society, Inc. A special thanks to David Adler, Ph.D., Department of Pathology, University of Washington, Seattle for the use of Idiogram Albums and for having the vision of creating a web site devoted to cytogenetics.

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  1. Division of Urology, Department of Surgery, The Research Institute of the McGill University Health Center, McGill University, Montreal, QC, Canada

    Mario Chevrette

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  1. Laure Humbert
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Correspondence to Mario Chevrette .

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  1. Dept. Oncology & Human Genetics, McGill University , Montreal, H2W 1S6, Canada

    William D. Foulkes

  2. Health System, University of Michigan, Ann Arbor, 48109, U.S.A.

    Kathleen A. Cooney

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Humbert, L., Chevrette, M. (2010). Somatic Molecular Genetics of Prostate Cancer. In: Foulkes, W., Cooney, K. (eds) Male Reproductive Cancers. Cancer Genetics. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-0449-2_5

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