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肿瘤休眠的免疫原性、细胞性和血管生成驱动因素——以黑色素瘤为例

Immunogenic, cellular, and angiogenic drivers of tumor dormancy--a melanoma view.

作者信息

Senft Daniela, Ronai Ze'ev A

机构信息

Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, USA.

出版信息

Pigment Cell Melanoma Res. 2016 Jan;29(1):27-42. doi: 10.1111/pcmr.12432. Epub 2015 Nov 27.

Abstract

In tumor cells, the ability to maintain viability over long time periods without proliferation is referred to as a state of dormancy. Maintenance of dormancy is controlled by numerous cellular and environmental factors, from immune surveillance and tumor-stroma interaction to intracellular signaling. Interference of dormancy (to an 'awaken' state) is associated with reduced response to therapy, resulting in relapse or in metastatic burst. Thus, maintaining a dormant state should prolong therapeutic responses and delay metastasis. Technical obstacles in studying tumor dormancy have limited our understanding of underlying mechanisms and hampered our ability to target dormant cells. In this review, we summarize the progress of research in the field of immunogenic, angiogenic, and cellular dormancy in diverse malignancies with particular attention to our current understanding in melanoma.

摘要

在肿瘤细胞中,长时间保持存活而不增殖的能力被称为休眠状态。休眠的维持受众多细胞和环境因素控制,从免疫监视、肿瘤-基质相互作用到细胞内信号传导。休眠的干扰(进入“唤醒”状态)与治疗反应降低相关,导致复发或转移爆发。因此,维持休眠状态应能延长治疗反应并延缓转移。研究肿瘤休眠的技术障碍限制了我们对潜在机制的理解,并阻碍了我们靶向休眠细胞的能力。在本综述中,我们总结了不同恶性肿瘤中免疫原性、血管生成性和细胞休眠领域的研究进展,特别关注我们目前对黑色素瘤的理解。

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