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首页> 外文期刊>Cancer Cell >Loss of ATM/Chk2/p53 pathway components accelerates tumor development and contributes to radiation resistance in gliomas.
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Loss of ATM/Chk2/p53 pathway components accelerates tumor development and contributes to radiation resistance in gliomas.

机译：ATM / Chk2 / p53通路成分的丢失加速了肿瘤的发展，并促进了神经胶质瘤的放射抵抗。

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摘要

Maintenance of genomic integrity is essential for adult tissue homeostasis and defects in the DNA-damage response (DDR) machinery are linked to numerous pathologies including cancer. Here, we present evidence that the DDR exerts tumor suppressor activity in gliomas. We show that genes encoding components of the DDR pathway are frequently altered in human gliomas and that loss of elements of the ATM/Chk2/p53 cascade accelerates tumor formation in a glioma mouse model. We demonstrate that Chk2 is required for glioma response to ionizing radiation in vivo and is necessary for DNA-damage checkpoints in the neuronal stem cell compartment. Finally, we observed that the DDR is constitutively activated in a subset of human GBMs, and such activation correlates with regions of hypoxia.
机译：维持基因组完整性对于成人组织的动态平衡至关重要，而DNA损伤反应（DDR）机制的缺陷则与包括癌症在内的众多病理因素有关。在这里，我们提供证据表明DDR在神经胶质瘤中发挥抑癌活性。我们表明，编码DDR通道的成分的基因在人类神经胶质瘤中经常发生变化，ATM / Chk2 / p53级联元件的缺失会加速神经胶质瘤小鼠模型中的肿瘤形成。我们证明Chk2是神经胶质瘤对体内电离辐射的反应所必需的，并且是神经元干细胞区室中DNA损伤检查点所必需的。最后，我们观察到DDR在人GBM的子集中被组成性激活，并且这种激活与缺氧区域相关。

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