作者: Mark R. Morris , Eamonn R. Maher
DOI: 10.1007/978-0-85729-482-1_3
关键词:
摘要: Cancer results from the accumulation of genetic (and epigenetic) alterations that causes dysregulation multiple intracellular and intercellular networks. In normal cells these networks ensure cellular proliferation tissue structure is tightly regulated. There are key tumour suppressor genes (TSG) such as p53 pRB protoncogenic RAS/RAF/MAPK cascade commonly dysregulated in many cancer types including genito-urinary cancers. This chapter describes how pathways contributes to specific cell attributes required for malignant progression. Moreover, their related disrupted cancers (such loss pVHL function clear Renal Cell Carcinoma (RCC) Androgen Receptor amplification prostate cancer) discussed detail. Our current understanding genetics molecular biology hereditary also described. While there germ-line gene mutations result inherited kidney (VHL, FLCN, SDHB) (BRCA2, HOXB13) high penetrance have yet be identified bladder testicular cancer.