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Oxidative stress and cancer pain

机译:氧化应激和癌症疼痛

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摘要

Breast cancers are the most common source of metastases to bone, of which cancer-induced bone pain is a frequent pathological feature. Cancer-induced bone pain is a unique pain state with multiple determinants that remains to be well understood and managed. Current standard treatments are limited by dose-dependent side effects that can reduce the quality of life of patients. Glutamate is a neurotransmitter and bone cell-signalling molecule that is released via the system x- C cystine/ glutamate antiporter from cancer cell types that frequently metastasize to bone, including breast cancers. In cancer cells, glutamate release is understood to be a side effect of the cellular response to oxidative stress that upregulates the expression and activity of system x- C to promote the increased import of cystine. Attenuation of glutamate release from cancer cells has been demonstrated to result in reductions in associated cancer-induced bone pain in animal models. This review examines the clinical implications of attenuating cystine uptake and glutamate release in the treatment of cancer-induced bone pain.
机译:乳腺癌是骨骼的最常见的转移来源,其中癌症诱导的骨疼痛是常见的病理特征。癌症诱导的骨疼痛是一种独特的疼痛状态,具有多种决定因素,其仍有待地理解和管理。目前的标准治疗受剂量依赖性副作用的限制,可以降低患者的寿命质量。谷氨酸是一种神经递质和骨细胞信号分子,可通过系统X-C胱氨酸/谷氨酸反常从癌细胞类型中释放,这些细胞类型经常转移到骨骼,包括乳腺癌。在癌细胞中,谷氨酸释放应理解为细胞反应对氧化应激的副作用,这使得促进系统X-C的表达和活性以促进胱氨酸的增加。已经证明了从癌细胞中抑制谷氨酸释放,导致动物模型中相关的癌症诱导的骨痛降低。本综述检测衰减胱氨酸摄取和谷氨酸释放治疗癌症诱导的骨疼痛的临床意义。

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