ASYMMETRIC CELL DIVISION: IMPLICATIONS FOR GLIOMA DEVELOPMENT AND TREATMENT.
ASYMMETRIC CELL DIVISION: IMPLICATIONS FOR GLIOMA DEVELOPMENT AND TREATMENT.
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DOI：
10.2478/s13380-013-0148-8
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发表时间：
2013-12
影响因子：
2.1
通讯作者：
Petritsch C
中科院分区：
文献类型：
--
作者：
Lewis KM;Petritsch C
胶质瘤是一种异质性疾病过程，具有不同的组织学和治疗反应。以前认为神经胶质瘤的组织学特征表明其细胞来源。然而，在正常成人脑中连续神经胶质细胞发生的发现和胶质瘤内脑肿瘤干细胞的鉴定导致了以下假设：这些脑肿瘤起源于多能神经干细胞或祖细胞，其主要在出生后期间不对称地分裂。不对称细胞分裂允许这些细胞类型同时自我更新，同时也产生用于分化途径的细胞。最近的研究表明，增加的对称细胞分裂，有利于自我更新途径，导致少突胶质细胞祖细胞形成少突胶质细胞瘤。相反，有证据表明星形细胞瘤中肿瘤干细胞样细胞的不对称细胞分裂维持可能导致获得治疗抗性。因此，正常脑干细胞和祖细胞的细胞分裂模式可能在设定肿瘤发生潜力和形成的肿瘤类型中起作用。此外，异质性肿瘤细胞群和它们各自的细胞分裂模式可赋予对治疗的不同敏感性。本文综述了细胞分裂模式的调控因子，这些调控因子可能是预防胶质瘤形成和提高治疗效果的治疗靶点。
Glioma is a heterogeneous disease process with differential histology and treatment response. It was previously thought that the histological features of glial tumors indicated their cell of origin. However, the discovery of continuous neuro-gliogenesis in the normal adult brain and the identification of brain tumor stem cells within glioma have led to the hypothesis that these brain tumors originate from multipotent neural stem or progenitor cells, which primarily divide asymmetrically during the postnatal period. Asymmetric cell division allows these cell types to concurrently self-renew whilst also producing cells for the differentiation pathway. It has recently been shown that increased symmetrical cell division, favoring the self-renewal pathway, leads to oligodendroglioma formation from oligodendrocyte progenitor cells. In contrast, there is some evidence that asymmetric cell division maintenance in tumor stem-like cells within astrocytoma may lead to acquisition of treatment resistance. Therefore cell division mode in normal brain stem and progenitor cells may play a role in setting tumorigenic potential and the type of tumor formed. Moreover, heterogeneous tumor cell populations and their respective cell division mode may confer differential sensitivity to therapy. This review aims to shed light on the controllers of cell division mode which may be therapeutically targeted to prevent glioma formation and improve treatment response.
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影响因子：
16.2
作者：
Bultje, Ronald S.;Castaneda-Castellanos, David R.;Jan, Lily Yen;Jan, Yuh-Nung;Kriegstein, Arnold R.;Shi, Song-Hai
通讯作者：
Shi, Song-Hai
影响因子：
3.4
作者：
Dai, Lan;He, Jintang;Liu, Yashu;Byun, Jaeman;Vivekanandan, Anuradha;Pennathur, Subramaniam;Fan, Xing;Lubman, David M.
通讯作者：
Lubman, David M.
影响因子：
4
作者：
Chang, Kai Chen;Wang, Cheng;Wang, Hongyan
通讯作者：
Wang, Hongyan
影响因子：
10.5
作者：
Dai, C;Celestino, JC;Holland, EC
通讯作者：
Holland, EC
影响因子：
3.6
作者：
Denysenko, Tetyana;Gennero, Luisa;Melcarne, Antonio
通讯作者：
Melcarne, Antonio