【摘要翻译】肿瘤抑制基因的失活：先天性还是后天性途径
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这篇文献讨论了肿瘤抑制基因的失活是先天性或后天性?可能对于我们研究泌尿系统肿瘤的发生有一定的意义.
【Journal】Cell Cycle. 2005 Jan 11;4(1) [Epub ahead of print] Related Articles, Links
【Title】Inactivation of Tumor Suppressor Genes: Choice Between Genetic and Epigenetic Routes.
【Author】Chen WY, Baylin SB.
Cancer Biology Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland, USA.
【Abstract】
Inactivation of tumor suppressor genes can occur via epigenetic or genetic mechanisms. The reasons underlying this choice of gene inactivation routes during tumorigenesis have not been clarified, nor have the precise roles in cancer evolution for genes which are solely affected by epigenetically mediated loss of function. Here we discuss a mouse model in which the disruption of Hic1, a gene solely involved with epigenetic silencing in human cancer, can markedly influence the disruption of the powerful tumor suppressor gene, p53, in determining malignant tumor incidence, spectrum and virulence. Furthermore, the mechanism for inactivation of Hic1 in tumors produced can be switched from an epigenetic to a genetic mode depending on how the Hic1 and p53 knockouts are localized on mouse chromosome 11. The value of such a model and the implications of the findings for choice of epigenetically versus genetically determined loss of gene function in cancer are discussed.
【翻译】
肿瘤抑制基因的失活:先天性还是后天性途径?
发生肿瘤抑制基因的失活可能是通过先天性或后天性途径.肿瘤的发生是先天性还是后天性途径,其原因仍未阐明,也没有对肿瘤生长过程中基因受到后天性的影响而功能丧失做出准确的估计.本文讨论的是一Hic1基因断裂的小鼠,Hic1基因和人类肿瘤后天性沉寂有关(此句翻译很拗口,欢迎各位有提出意见).并能显著影响肿瘤抑制基因P53的断裂,P53基因决定了恶性肿瘤的发生率,光谱和毒力.而且,肿瘤Hic1基因失活的机制能从后天性模式转化为先天性模式,这取决于小鼠11号染色体上Hic1基因和p53基因的定位.这样的小鼠模型和研究结果对肿瘤中基因功能丧失的是先天还是后天性的价值目前仍在讨论当中。
【全文】
http://www.dxy.cn/bbs/user/download/2421510/chenCC4-1%5B1%5D.pdf
【Journal】Cell Cycle. 2005 Jan 11;4(1) [Epub ahead of print] Related Articles, Links
【Title】Inactivation of Tumor Suppressor Genes: Choice Between Genetic and Epigenetic Routes.
【Author】Chen WY, Baylin SB.
Cancer Biology Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland, USA.
【Abstract】
Inactivation of tumor suppressor genes can occur via epigenetic or genetic mechanisms. The reasons underlying this choice of gene inactivation routes during tumorigenesis have not been clarified, nor have the precise roles in cancer evolution for genes which are solely affected by epigenetically mediated loss of function. Here we discuss a mouse model in which the disruption of Hic1, a gene solely involved with epigenetic silencing in human cancer, can markedly influence the disruption of the powerful tumor suppressor gene, p53, in determining malignant tumor incidence, spectrum and virulence. Furthermore, the mechanism for inactivation of Hic1 in tumors produced can be switched from an epigenetic to a genetic mode depending on how the Hic1 and p53 knockouts are localized on mouse chromosome 11. The value of such a model and the implications of the findings for choice of epigenetically versus genetically determined loss of gene function in cancer are discussed.
【翻译】
肿瘤抑制基因的失活:先天性还是后天性途径?
发生肿瘤抑制基因的失活可能是通过先天性或后天性途径.肿瘤的发生是先天性还是后天性途径,其原因仍未阐明,也没有对肿瘤生长过程中基因受到后天性的影响而功能丧失做出准确的估计.本文讨论的是一Hic1基因断裂的小鼠,Hic1基因和人类肿瘤后天性沉寂有关(此句翻译很拗口,欢迎各位有提出意见).并能显著影响肿瘤抑制基因P53的断裂,P53基因决定了恶性肿瘤的发生率,光谱和毒力.而且,肿瘤Hic1基因失活的机制能从后天性模式转化为先天性模式,这取决于小鼠11号染色体上Hic1基因和p53基因的定位.这样的小鼠模型和研究结果对肿瘤中基因功能丧失的是先天还是后天性的价值目前仍在讨论当中。
【全文】
http://www.dxy.cn/bbs/user/download/2421510/chenCC4-1%5B1%5D.pdf
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