抗细胞因子和抗细胞因子受体治疗对实验性癌症恶病质的抑制作用。

Cytokines and molecular therapy Pub Date : 1995-06-01
G Strassmann, T Kambayashi
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引用次数: 0

摘要

恶病质包括癌症患者发生的一系列代谢变化,包括肌肉和脂肪组织减少、虚弱、厌食症、低血糖和高钙血症。这些症状使治疗干预复杂化并降低患者的生活质量。本文综述了细胞因子在癌症恶病质中的作用,并阐述了IL-6等细胞因子在携带c -26小鼠的消耗中的作用。通过抗体中和IL-6或苏拉明拮抗IL-6受体,可显著降低恶病质关键参数的严重程度。其他几个因子(PGE2, IL-1, IL-10和tnf - α)在C-26肿瘤细胞和肿瘤浸润性巨噬细胞之间的细胞通讯中的参与也被描述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inhibition of experimental cancer cachexia by anti-cytokine and anti-cytokine-receptor therapy.

Cachexia consists of a constellation of metabolic changes that occur in cancer patients, including the reduction of muscle and fat tissue, asthenia, anorexia, hypoglycemia and hypercalcemia. These syndromes complicate therapeutic intervention and decrease the quality of life of the patient. This review discusses the involvement of cytokines in cancer cachexia and describes the contribution of IL-6 and other cytokines to the wasting of C-26-bearing mice. The neutralization of IL-6 by antibody, or IL-6 receptor antagonism by suramin, significantly reduce the severity of key parameters of cachexia. The participation of several other factors (PGE2, IL-1, IL-10 and TNF-alpha) in the cellular communication between the C-26 tumor cell and tumor-infiltrating macrophages is also described.

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