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Genetics and Genito-Urinary Cancer

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Urological Oncology

Abstract

Cancer results from the accumulation of genetic (and epigenetic) alterations that causes the dysregulation of multiple intracellular and intercellular networks. In normal cells these networks ensure cellular proliferation and tissue structure is tightly regulated. There are key tumour suppressor genes (TSG) and networks such as the p53 and pRB networks and protoncogenic networks such as the RAS/RAF/MAPK cascade that are commonly dysregulated in many cancer types including genito-urinary cancers. This chapter describes how dysregulation of these pathways contributes to specific tumour cell attributes required for malignant progression. Moreover, genes and their related networks that are disrupted in specific genito-urinary cancers (such as the loss of pVHL function in clear cell Renal Cell Carcinoma (RCC) and Androgen Receptor amplification in prostate cancer) are discussed in detail. Our current understanding of the genetics and molecular biology of hereditary genito-urinary cancers is also described. While there are specific germ-line gene mutations that result in inherited kidney cancer (VHL, FLCN, SDHB) and prostate cancer (BRCA2, HOXB13) specific high penetrance gene mutations have yet to be identified in hereditary bladder cancer and testicular cancer.

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Correspondence to Mark R. Morris PhD, BSc .

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Morris, M.R., Maher, E.R. (2015). Genetics and Genito-Urinary Cancer. In: Nargund, V., Raghavan, D., Sandler, H. (eds) Urological Oncology. Springer, London. https://doi.org/10.1007/978-0-85729-482-1_3

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