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MSH6 inactivation and emergent temozolomide resistance in human glioblastomas.

作者信息

Cahill Daniel P, Codd Patrick J, Batchelor Tracy T, Curry William T, Louis David N

机构信息

Neurosurgical Service, Massachusetts General Hospital, Harvard Medical School, Boston, USA.

出版信息

Clin Neurosurg. 2008;55:165-71.

PMID:19248684
Abstract
摘要

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MSH6 inactivation and emergent temozolomide resistance in human glioblastomas.人胶质母细胞瘤中MSH6失活与新出现的替莫唑胺耐药性
Clin Neurosurg. 2008;55:165-71.
2
Loss of the mismatch repair protein MSH6 in human glioblastomas is associated with tumor progression during temozolomide treatment.人胶质母细胞瘤中错配修复蛋白MSH6的缺失与替莫唑胺治疗期间的肿瘤进展相关。
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[Temozolomide in patients with a glioblastoma multiforme: new developments].[替莫唑胺治疗多形性胶质母细胞瘤患者：新进展]
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Adjuvant temozolomide: how long and how much?辅助性替莫唑胺：疗程多久及剂量多少？
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Treatment of brain tumors.脑肿瘤的治疗。
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Early clinical and neuroradiological worsening after radiotherapy and concomitant temozolomide in patients with glioblastoma: tumour progression or radionecrosis?胶质母细胞瘤患者放疗联合替莫唑胺治疗后早期临床及神经放射学恶化：肿瘤进展还是放射性坏死？
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Temozolomide in glioblastoma multiforme of the elderly.替莫唑胺用于老年多形性胶质母细胞瘤的治疗
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Molecular mechanisms of temozolomide resistance in glioblastoma multiforme.胶质母细胞瘤中替莫唑胺耐药的分子机制。
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MSH6 mutations arise in glioblastomas during temozolomide therapy and mediate temozolomide resistance.MSH6突变在替莫唑胺治疗期间出现在胶质母细胞瘤中，并介导替莫唑胺耐药。
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Recycling drug screen repurposes hydroxyurea as a sensitizer of glioblastomas to temozolomide targeting de novo DNA synthesis, irrespective of molecular subtype.药物再利用筛选将羟基脲重新用作替莫唑胺增敏剂，针对新合成的 DNA，而与分子亚型无关。
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