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治疗转移的新兴策略。

Emerging strategies for treating metastasis.

作者信息

Esposito Mark, Ganesan Shridar, Kang Yibin

机构信息

Department of Molecular Biology, Princeton University, Princeton, NJ, USA.

Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.

出版信息

Nat Cancer. 2021 Mar;2(3):258-270. doi: 10.1038/s43018-021-00181-0. Epub 2021 Mar 24.

DOI:10.1038/s43018-021-00181-0
PMID:33899000
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8064405/
Abstract

The systemic spread of tumor cells is the ultimate cause of the majority of deaths from cancer, yet few successful therapeutic strategies have emerged to specifically target metastasis. Here we discuss recent advances in our understanding of tumor-intrinsic pathways driving metastatic colonization and therapeutic resistance, as well as immune activating strategies to target metastatic disease. We focus on therapeutically exploitable mechanisms, promising strategies in preclinical and clinical development, and emerging areas with potential to become innovative treatments.

摘要

肿瘤细胞的全身扩散是大多数癌症死亡的最终原因,但针对转移的特异性治疗策略却很少成功出现。在此,我们讨论了在理解驱动转移定植和治疗抗性的肿瘤内在途径方面的最新进展,以及针对转移性疾病的免疫激活策略。我们关注可用于治疗的机制、临床前和临床开发中的有前景的策略,以及有可能成为创新疗法的新兴领域。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/f0e2095ca1d6/nihms-1684791-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/93250995fa54/nihms-1684791-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/ae11f078aabe/nihms-1684791-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/0425c080d512/nihms-1684791-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/f0e2095ca1d6/nihms-1684791-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/93250995fa54/nihms-1684791-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/ae11f078aabe/nihms-1684791-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/0425c080d512/nihms-1684791-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a723/8064405/f0e2095ca1d6/nihms-1684791-f0004.jpg

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Accumulation of long-chain fatty acids in the tumor microenvironment drives dysfunction in intrapancreatic CD8+ T cells.
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