Sudarshan Sunil, Pinto Peter A, Neckers Len, Linehan W Marston
Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-1107, USA.
Nat Clin Pract Urol. 2007 Feb;4(2):104-10. doi: 10.1038/ncpuro0711.
Renal cell carcinoma (RCC) represents a group of diseases linked by their primary site of origin, the kidney. Studies of families with a genetic predisposition to the development of kidney cancer have revealed that multiple genes are involved in the molecular pathogenesis of RCC. Germline mutations in a gene that encodes a Krebs cycle enzyme have been found to result in a distinct clinical entity referred to as hereditary leiomyomatosis and renal cell cancer (HLRCC). HLRCC is inherited in an autosomal-dominant fashion. Affected individuals in HLRCC families are at risk for the development of leiomyomas of the skin and uterus as well as renal cancers. HLRCC-associated kidney tumors are often biologically aggressive. Linkage analysis has identified germline alterations in the fumarate hydratase (FH) gene associated with HLRCC. While the mechanisms of molecular carcinogenesis are not entirely understood, several lines of evidence derived from clinical and basic research suggest that pseudohypoxia might drive cellular transformation. The role of FH mutations in sporadic tumors seems to be limited. Nevertheless, continued investigation of HLRCC should provide further insight into the mechanisms of kidney cancer development, and could potentially identify targets for new therapeutic approaches to RCC.
肾细胞癌(RCC)是一组起源于肾脏这一主要部位的疾病。对有患肾癌遗传易感性的家族进行的研究表明,多个基因参与了肾细胞癌的分子发病机制。已发现编码三羧酸循环酶的基因中的种系突变会导致一种独特的临床实体,称为遗传性平滑肌瘤病和肾细胞癌(HLRCC)。HLRCC以常染色体显性方式遗传。HLRCC家族中的受影响个体有患皮肤和子宫平滑肌瘤以及肾癌的风险。与HLRCC相关的肾肿瘤通常在生物学上具有侵袭性。连锁分析已确定与HLRCC相关的延胡索酸水合酶(FH)基因中的种系改变。虽然分子致癌机制尚未完全了解,但来自临床和基础研究的几条证据表明,假性低氧可能驱动细胞转化。FH突变在散发性肿瘤中的作用似乎有限。尽管如此,对HLRCC的持续研究应能进一步深入了解肾癌的发展机制,并有可能确定肾细胞癌新治疗方法的靶点。