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肿瘤衰老:来自小鼠和人类的证据。

Senescence in tumours: evidence from mice and humans.

机构信息

Spanish National Cancer Research Centre, Madrid, Spain.

出版信息

Nat Rev Cancer. 2010 Jan;10(1):51-7. doi: 10.1038/nrc2772.

DOI:10.1038/nrc2772
PMID:20029423
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3672965/
Abstract

The importance of cellular senescence, which is a stress response that stably blocks proliferation, is increasingly being recognized. Senescence is prevalent in pre-malignant tumours, and progression to malignancy requires evading senescence. Malignant tumours, however, may still undergo senescence owing to interventions that restore tumour suppressor function or inactivate oncogenes. Senescent tumour cells can be cleared by immune cells, which may result in efficient tumour regression. Standard chemotherapy also has the potential to induce senescence, which may partly underlie its therapeutic activity. Although these concepts are well supported in mouse models, translating them to clinical oncology remains a challenge.

摘要

细胞衰老作为一种稳定阻止增殖的应激反应,其重要性正日益受到重视。衰老普遍存在于恶性前期肿瘤中,而向恶性肿瘤的进展则需要逃避衰老。然而,由于恢复肿瘤抑制功能或失活癌基因的干预,恶性肿瘤仍可能发生衰老。衰老的肿瘤细胞可以被免疫细胞清除,这可能导致肿瘤的有效消退。标准的化疗也有可能诱导衰老,这可能是其治疗活性的部分基础。尽管这些概念在小鼠模型中得到了很好的支持,但将其转化为临床肿瘤学仍然是一个挑战。

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本文引用的文献

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Nat Rev Cancer. 2009 Dec;9(12):862-73. doi: 10.1038/nrc2763.
2
p53 isoforms Delta133p53 and p53beta are endogenous regulators of replicative cellular senescence.p53 异构体 Delta133p53 和 p53β 是复制性细胞衰老的内源性调节因子。
Nat Cell Biol. 2009 Sep;11(9):1135-42. doi: 10.1038/ncb1928. Epub 2009 Aug 23.
3
Real-time in vivo imaging of p16Ink4a reveals cross talk with p53.p16Ink4a的实时体内成像揭示了与p53的相互作用。
J Cell Biol. 2009 Aug 10;186(3):393-407. doi: 10.1083/jcb.200904105.
4
Endogenous expression of Hras(G12V) induces developmental defects and neoplasms with copy number imbalances of the oncogene.Hras(G12V)的内源性表达会诱导发育缺陷和肿瘤形成,并伴有癌基因的拷贝数失衡。
Proc Natl Acad Sci U S A. 2009 May 12;106(19):7979-84. doi: 10.1073/pnas.0900343106. Epub 2009 Apr 29.
5
Melanocytic nevus-like hyperplasia and melanoma in transgenic BRAFV600E mice.转基因BRAFV600E小鼠中的黑素细胞痣样增生和黑色素瘤
Oncogene. 2009 Jun 11;28(23):2289-98. doi: 10.1038/onc.2009.95. Epub 2009 Apr 27.
6
Oncogenic Braf induces melanocyte senescence and melanoma in mice.致癌性Braf在小鼠中诱导黑素细胞衰老和黑色素瘤。
Cancer Cell. 2009 Apr 7;15(4):294-303. doi: 10.1016/j.ccr.2009.02.022.
7
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Cancer Cell. 2009 Apr 7;15(4):255-69. doi: 10.1016/j.ccr.2009.03.001.
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Expression of H-RASV12 in a zebrafish model of Costello syndrome causes cellular senescence in adult proliferating cells.在斑马鱼科斯特洛综合征模型中,H-RASV12的表达会导致成年增殖细胞发生细胞衰老。
Dis Model Mech. 2009 Jan-Feb;2(1-2):56-67. doi: 10.1242/dmm.001016. Epub 2008 Dec 22.
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