The molecular genetics of prostate cancer
The molecular genetics of prostate cancer
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DOI：
10.1016/s0090-4295(03)00776-3
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发表时间：
2003-11-01
期刊：
影响因子：
2.1
通讯作者：
Visakorpi, T
中科院分区：
文献类型：
--
作者：
Visakorpi, T
前列腺癌是男性癌症相关死亡的第二大常见原因，其分子遗传学知之甚少。遗传因素被认为占前列腺癌风险的42%，尽管已经鉴定了多个染色体易感基因座，但这些基因座的靶基因尚未明确。其异质性表明，前列腺癌的易感性可能涉及多个基因和可变的表型表达。已发现在前列腺癌进展中发挥作用的基因包括GST 1和PTEN，以及雄激素受体（AR）基因。有证据表明，当雄激素水平较低时，AR信号通路可以被其他配体激活。最近的研究结果还涉及Kruppel样因子6（KFL 6），E-钙粘蛋白，真核生物翻译起始因子的p40亚基（eIF 3-p40），和Elongin C，但需要证实的证据来阐明这些因子的作用。技术的进步，如互补DNA和组织微阵列，促进了遗传变异的鉴定和功能的研究，但仍然需要改进的搜索和分析基因的工具。
The molecular genetics of prostate cancer, the second most common cause of cancer-related death in men, is poorly understood. Inherited factors are believed to account for 42% of the risk of prostate cancer, and although multiple chromosomal loci of susceptibility have been identified, the target genes for these loci have not been well defined. Its heterogeneous nature suggests that the predisposition to prostate cancer may involve multiple genes and variable phenotypic expression. Genes that have been found to play a role in progression of prostate cancer include GSTP1 and PTEN, as well as the androgen receptor (AR) gene. Evidence suggests that the AR signaling pathway can be activated by other ligands when androgen levels are low. Recent findings have also implicated Kruppel-like factor 6 (KFL6), E-cadherin, the p40 subunit of eukaryotic translation initiation factor (elF3-p40), and Elongin C, but confirmatory evidence is required to clarify the roles of these factors. Technologic advances, such as complementary DNA and tissue microarrays, have facilitated identification of genetic alterations and investigations of their function, but improved tools for searching and analyzing genes are still needed.