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Epithelial-to-mesenchymal transition in cancer: complexity and opportunities.癌症中的上皮-间充质转化:复杂性和机遇。
Front Med. 2018 Aug;12(4):361-373. doi: 10.1007/s11684-018-0656-6. Epub 2018 Jul 24.
2
Mitotic polarization of transcription factors during asymmetric division establishes fate of forming cancer cells.有丝分裂过程中转录因子的极性不对称分裂建立了形成癌细胞的命运。
Nat Commun. 2018 Jun 21;9(1):2424. doi: 10.1038/s41467-018-04663-1.
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Epigenetic Priming in Cancer Initiation.癌症起始中的表观遗传预激发
Trends Cancer. 2018 Jun;4(6):408-417. doi: 10.1016/j.trecan.2018.04.007.
4
Notch ligand Dll1 mediates cross-talk between mammary stem cells and the macrophageal niche.Notch 配体 Dll1 介导乳腺干细胞与巨噬细胞生态位之间的串扰。
Science. 2018 Jun 29;360(6396). doi: 10.1126/science.aan4153. Epub 2018 May 17.
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The epigenetic basis of cellular plasticity.细胞可塑性的表观遗传学基础。
Curr Opin Cell Biol. 2017 Dec;49:116-122. doi: 10.1016/j.ceb.2018.01.003. Epub 2018 Feb 4.
6
Symmetry from Asymmetry or Asymmetry from Symmetry?不对称产生对称还是对称产生不对称?
Cold Spring Harb Symp Quant Biol. 2017;82:305-318. doi: 10.1101/sqb.2017.82.034272. Epub 2018 Jan 18.
7
Cancer stem cells revisited.癌症干细胞再探。
Nat Med. 2017 Oct 6;23(10):1124-1134. doi: 10.1038/nm.4409.
8
Epithelial-to-Mesenchymal Transition: Epigenetic Reprogramming Driving Cellular Plasticity.上皮-间充质转化:表观遗传重编程驱动细胞可塑性。
Trends Genet. 2017 Dec;33(12):943-959. doi: 10.1016/j.tig.2017.08.004. Epub 2017 Sep 14.
9
Putting p53 in Context.将p53置于背景中考虑。
Cell. 2017 Sep 7;170(6):1062-1078. doi: 10.1016/j.cell.2017.08.028.
10
Fate mapping of human glioblastoma reveals an invariant stem cell hierarchy.人类胶质母细胞瘤的命运图谱揭示了一种不变的干细胞层级结构。
Nature. 2017 Sep 14;549(7671):227-232. doi: 10.1038/nature23666. Epub 2017 Aug 30.

表观遗传上不同的姐妹染色单体和肿瘤起始细胞的不对称产生。

Epigenetically distinct sister chromatids and asymmetric generation of tumor initiating cells.

机构信息

a Molecular Targets Program , James Graham Brown Cancer Center , Louisville , Kentucky.

b Department of Ophthalmology and Visual Sciences.

出版信息

Cell Cycle. 2018;17(18):2221-2229. doi: 10.1080/15384101.2018.1532254. Epub 2018 Oct 13.

DOI:10.1080/15384101.2018.1532254
PMID:30290712
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6226223/
Abstract

Cancer stem cells (CSC) are thought to be an important source of cancer cells in tumors of different origins. Mounting evidence suggests they are generated reversibly from existing cancer cells, and supply new cancer cells during tumor progression and following therapy. Elegant lineage mapping stud(ies are identifying progenitors, and in some cases differentiated cells, as targets of transformation in a variety of tumors. Recent evidence suggests resulting tumor initiating cells (TIC) might be distinct from CSC. Molecular pathways leading from cells of tumor origin to precancerous lesions and cancer cells are only beginning to be unraveled. We review a pathway where asymmetric division of precancerous cells generates TIC in a K-Ras-initiated model of lung cancer. And, we compare unexpected steps in this asymmetric division to those evident in well-studied stem cell models.

摘要

癌症干细胞(CSC)被认为是不同来源肿瘤中癌细胞的重要来源。越来越多的证据表明,它们可以从现有癌细胞中可逆地产生,并在肿瘤进展和治疗后提供新的癌细胞。精心设计的谱系追踪研究正在确定祖细胞,在某些情况下还确定了分化细胞,作为各种肿瘤转化的靶点。最近的证据表明,由此产生的肿瘤起始细胞(TIC)可能与 CSC 不同。从肿瘤起源细胞到癌前病变和癌细胞的分子途径才刚刚开始被揭示。我们回顾了一条途径,即癌前细胞的不对称分裂在 K-Ras 引发的肺癌模型中产生了 TIC。并且,我们将这种不对称分裂中的意外步骤与在研究充分的干细胞模型中出现的步骤进行了比较。