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【bio-news】CHD5 Is a Tumor Suppressor at Human 1p36
Cancer gene discovery has relied extensively on analyzing tumors for gains and losses to reveal the location of oncogenes and tumor suppressor genes, respectively. Deletions of 1p36 are extremely common genetic lesions in human cancer, occurring in malignancies of epithelial, neural, and hematopoietic origin. Although this suggests that 1p36 harbors a gene that drives tumorigenesis when inactivated, the identity of this tumor suppressor has remained elusive. Here we use chromosome engineering to generate mouse models with gain and loss of a region corresponding to human 1p36. This approach functionally identifies chromodomain helicase DNA binding domain 5 (Chd5) as a tumor suppressor that controls proliferation, apoptosis, and senescence via the p19Arf/p53 pathway. We demonstrate that Chd5 functions as a tumor suppressor in vivo and implicate deletion of CHD5 in human cancer. Identification of this tumor suppressor provides new avenues for exploring innovative clinical interventions for cancer. 我认领 Cancer gene discovery has relied extensively on analyzing tumors for gains and losses to reveal the location of oncogenes and tumor suppressor genes, respectively.
癌症基因的发现在很大程度上依赖于对肿瘤的获得或丢失基因进行分析以定位癌基因和抑癌基因。
Deletions of 1p36 are extremely common genetic lesions in human cancer, occurring in malignancies of epithelial, neural, and hematopoietic origin.
1p36缺失是发生于上皮、神经、造血恶性肿瘤中非常常见的基因损伤。
Although this suggests that 1p36 harbors a gene that drives tumorigenesis when inactivated, the identity of this tumor suppressor has remained elusive.
因此提示：1p36存在一种基因，当它灭活时，能促进肿瘤发生。但这种抑癌基因仍未能确定。
Here we use chromosome engineering to generate mouse models with gain and loss of a region corresponding to human 1p36.
这里，我们通过染色体工程的方法制作获得或缺失与人1p36区域相当的区域的小鼠模型。
This approach functionally identifies chromodomain helicase DNA binding domain 5 (Chd5) as a tumor suppressor that controls proliferation, apoptosis, and senescence via the p19Arf/p53 pathway.
通过这种方法将染色质域解旋酶DNA结合区5 (Chd5)定义为经p19Arf/p53途径控制增殖、凋亡、老化的抑癌基因。
We demonstrate that Chd5 functions as a tumor suppressor in vivo and implicate deletion of CHD5 in human cancer. Identification of this tumor suppressor provides new avenues for exploring innovative clinical interventions for cancer.
我们证明Chd5在活体中作为抑癌基因发挥作用而且在人类恶性肿瘤与CHD5的缺失有关。此抑癌基因的确定为探索肿瘤新的临床干预提供了新的途径。
编译如下：
癌症基因的发现在很大程度上依赖于对肿瘤的获得或丢失基因进行分析以定位癌基因和抑癌基因。1p36缺失是发生于上皮、神经、造血恶性肿瘤中非常常见的基因损伤。因此提示：1p36存在一种基因，当它灭活时能促进肿瘤发生，但这种抑癌基因仍未能确定。这里，我们通过染色体工程的方法制作与人1p36区域相当的区域获得或缺失的小鼠模型。通过这种方法将染色质域解旋酶DNA结合区5 (Chd5)定义为经p19Arf/p53途径控制增殖、凋亡、老化的抑癌基因。我们证明Chd5在活体中作为抑癌基因发挥作用，而且人类的恶性肿瘤与CHD5的缺失有关。此抑癌基因的确定为探索肿瘤的临床干预提供了新的途径。 [标签:content1][标签:content2]
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作者:admin@医学,生命科学 2011-02-15 17:11
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