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肿瘤细胞休眠

Tumor cell dormancy.

作者信息

Gomis Roger R, Gawrzak Sylwia

机构信息

Oncology Program, Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain; ICREA Institució Catalana de Recerca i Estudis Avançats, 08010 Barcelona, Spain.

Oncology Program, Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain.

出版信息

Mol Oncol. 2017 Jan;11(1):62-78. doi: 10.1016/j.molonc.2016.09.009. Epub 2016 Oct 7.

DOI:10.1016/j.molonc.2016.09.009
PMID:28017284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5423221/
Abstract

Metastasis is the primary cause of death in cancer patients and current treatments fail to provide durable responses. Efforts to treat metastatic disease are hindered by the fact that metastatic cells often remain dormant for prolonged intervals of years, or even decades. Tumor dormancy reflects the capability of disseminated tumor cells (DTCs), or micrometastases, to evade treatment and remain at low numbers after primary tumor resection. Unfortunately, dormant cells will eventually produce overt metastasis. Innovations are needed to understand metastatic dormancy and improve cancer detection and treatment. Currently, few models exist that faithfully recapitulate metastatic dormancy and metastasis to clinically relevant tissues, such as the bone. Herein, we discuss recent advances describing genetic cell-autonomous and systemic or local changes in the microenvironment that have been shown to endow DTCs with properties to survive and eventually colonize distant organs.

摘要

转移是癌症患者死亡的主要原因,目前的治疗方法无法提供持久的疗效。转移性疾病的治疗受到以下事实的阻碍:转移细胞通常会在数年甚至数十年的长时间内保持休眠状态。肿瘤休眠反映了播散性肿瘤细胞(DTCs)或微转移灶逃避治疗并在原发性肿瘤切除后保持低数量的能力。不幸的是,休眠细胞最终会产生明显的转移。需要创新来理解转移性休眠并改善癌症的检测和治疗。目前,很少有模型能够如实地重现转移性休眠以及向临床相关组织(如骨骼)的转移。在此,我们讨论了最近的进展,这些进展描述了基因细胞自主性以及微环境中的系统性或局部变化,这些变化已被证明赋予DTCs存活并最终在远处器官定植的特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/1118813bfca5/MOL2-11-62-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/4202f0d5546a/MOL2-11-62-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/a8a14925e56d/MOL2-11-62-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/6108f3830522/MOL2-11-62-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/ab79294e0a62/MOL2-11-62-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/a7288e8823fa/MOL2-11-62-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/1118813bfca5/MOL2-11-62-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/4202f0d5546a/MOL2-11-62-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/a8a14925e56d/MOL2-11-62-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/6108f3830522/MOL2-11-62-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/ab79294e0a62/MOL2-11-62-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/a7288e8823fa/MOL2-11-62-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad58/5423221/1118813bfca5/MOL2-11-62-g006.jpg

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本文引用的文献

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The metabolic co-regulator PGC1α suppresses prostate cancer metastasis.代谢协同调节因子PGC1α可抑制前列腺癌转移。
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