Stat3-driven cancer-related inflammation as a key therapeutic target for cancer immunotherapy.
Stat3-driven cancer-related inflammation as a key therapeutic target for cancer immunotherapy.
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DOI：
10.2217/imt.11.26
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发表时间：
2011-05
期刊：
影响因子：
2.8
通讯作者：
Takuma Kato
中科院分区：
文献类型：
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作者：
Takuma Kato
发育和生长分为独立或依次的三个阶段：宿主免疫系统识别并消除原发性肿瘤（癌症免疫监视），抑制已形成肿瘤的生长以使其在临床上不明显（平衡），并失去对抑制免疫原性和/或获得颠覆免疫系统能力的肿瘤细胞变异的控制（逃逸）。最近的几项人类癌症研究也提供了间接证据，表明免疫编辑可能在多种人类恶性肿瘤中发挥作用。看来任何旨在消除临床上明显的肿瘤的免疫治疗策略从表面上看可能都是不成功的，因为肿瘤已经过编辑，因此它们对免疫攻击具有高度抵抗力。然而，通过癌症疫苗和/或过继性免疫疗法结合阻断免疫抑制机制来增强对肿瘤的免疫力预计将具有治疗功效。
development and growth by three phases either independently or in sequence: the host immune system recognizes and eliminates primary developing tumors (cancer immunosurveillance), restrains the growth of established tumors to keep them clinically unapparent (equilibrium), and loses control of tumor cell variants that dampen immunogenicity and/or gain the capacity to subvert immune system (escape). Several recent studies in human cancer also provide circumstantial evidence to indicate that immunoediting might be operative in diverse human malignancies. It appears that any immunotherapeutic strategies aimed at eliminating clinically apparent tumors might be unsuccessful on the surface, because the tumors have been edited so that they are highly resistant to immune attack. However, intensifying immunity to tumors by cancer vaccines and/or adoptive immunotherapy in combination with blocking immunosuppressive mechanisms would be expected to have therapeutic efficacies.