Cellular reprogramming in skin cancer.
Cellular reprogramming in skin cancer.
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DOI：
10.1016/j.semcancer.2014.03.006
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发表时间：
2015-06
影响因子：
14.5
通讯作者：
Balmain A
中科院分区：
文献类型：
--
作者：
Song IY;Balmain A
早期原始干细胞由于具有自我更新和寿命长的内在特征，一直被认为是肿瘤的起源细胞（肿瘤起始靶细胞）。然而，新出现的证据表明，由于组织损伤导致炎症和伤口愈合，正常的承诺细胞在重编程时具有惊人的能力，可以作为储备干细胞。这导致了另一种观点，即肿瘤可能起源于分化的细胞，这些细胞可以通过遗传或表观遗传重编程重新获得干细胞特性。很可能这两种模型都是正确的，并且存在连续的潜在细胞起源，从早期原始干细胞到固定的祖细胞甚至是终末分化细胞。靶细胞的性质和引入的特定类型的基因突变的结合决定了肿瘤细胞谱系，以及恶性转化的潜力。来自小鼠皮肤癌变模型的证据表明，干细胞层次中不同阶段的初始细胞对重编程的需求程度不同（例如炎症刺激），这取决于它们的分化程度。这篇文章将提出证据支持这些概念，这些概念是从几种小鼠皮肤癌模型的研究中发展出来的。
Early primitive stem cells have long been viewed as the cancer cells of origin (tumor initiating target cells) due to their intrinsic features of self-renewal and longevity. However, emerging evidence suggests a surprising capacity for normal committed cells to function as reserve stem cells upon reprogramming as a consequence of tissue damage resulting in inflammation and wound healing. This results in an alternative concept positing that tumors may originate from differentiated cells that can re-acquire stem cell properties due to genetic or epigenetic reprogramming. It is likely that both models are correct, and that a continuum of potential cells of origin exists, ranging from early primitive stem cells to committed progenitor or even terminally differentiated cells. A combination of the nature of the target cell and the specific types of gene mutations introduced determine tumor cell lineage, as well as potential for malignant conversion. Evidence from mouse skin models of carcinogenesis suggests that initiated cells at different stages within a stem cell hierarchy have varying degrees of requirement for reprogramming (e.g. inflammation stimuli), depending on their degree of differentiation. This article will present evidence in favor of these concepts that has been developed from studies of several mouse models of skin carcinogenesis.
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影响因子：
21.3
作者：
通讯作者：
--
肿瘤基因对神经元和星形胶质细胞的去分化会在小鼠中诱导神经胶质瘤。
DOI：
10.1126/science.1226929
发表时间：
2012-11-23
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Friedmann-Morvinski D;Bushong EA;Ke E;Soda Y;Marumoto T;Singer O;Ellisman MH;Verma IM
通讯作者：
Verma IM
影响因子：
64.8
作者：
Buczacki, Simon J. A.;Zecchini, Heather Ireland;Winton, Douglas J.
通讯作者：
Winton, Douglas J.
影响因子：
64.8
作者：
AKHURST, RJ;FEE, F;BALMAIN, A
通讯作者：
BALMAIN, A
影响因子：
64.8
作者：
BALMAIN, A;RAMSDEN, M;SMITH, J
通讯作者：
SMITH, J