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肿瘤易感性与中枢神经上皮细胞发生及胶质瘤分化的相关性。

The correlation of neoplastic vulnerability with central neuroepithelial cytogeny and glioma differentiation.

作者信息

Rubinstein L J

出版信息

J Neurooncol. 1987;5(1):11-27. doi: 10.1007/BF00162761.

DOI:10.1007/BF00162761
PMID:3037035
Abstract

The vulnerability of neuroepithelial cells in the central nervous system (CNS) to neoplastic transformation results from the interaction of several factors: the existence of a reserve population of stem cells, the capability of differentiated cells to reenter the kinetic cycle, the number of replicating cells at risk at a particular time, the length of time during which a particular cell population remains in the cycle, the state of differentiation and the further differentiation potential of that population, and the steps of differentiation that are achieved in successive cell generations. This concept explains many aspects of CNS tumor incidence and the relationship of central neuroepithelial embryonal tumors to tumors of adult cell type. The incidence of different types of central neuroepithelial tumors can be correlated with the width of the window of neoplastic vulnerability. Examples illustrating the existence of only a narrow window include such rare tumors as medulloepitheliomas, cerebral neuroblastomas, gangliogliomas and ependymoblastomas. By contrast, cerebellar medulloblastomas, astrocytomas, mixed astrocytomas and oligodendrogliomas, and glioblastomas exemplify instances in which a relatively wider window of vulnerability exists in the light of cellular neuro-ontogeny and of the capacity of glial cells for postnatal replication. The relationship that may occasionally be established between the development of a glioma and the production of cellular gliosis such as may follow brain injury or accompany multiple sclerosis can also be viewed in the light of that concept. Increasing awareness is needed concerning the development of postradiation gliomas, in particular after the apparently successful treatment of acute lymphocytic leukemia.

摘要

中枢神经系统(CNS)中神经上皮细胞发生肿瘤转化的易感性是由多种因素相互作用导致的:存在干细胞储备群体、分化细胞重新进入动力学周期的能力、特定时间处于危险中的复制细胞数量、特定细胞群体在周期中停留的时间长度、该群体的分化状态和进一步分化潜力,以及连续细胞世代中实现的分化步骤。这一概念解释了CNS肿瘤发生率的许多方面以及中枢神经上皮胚胎性肿瘤与成人细胞类型肿瘤的关系。不同类型的中枢神经上皮肿瘤的发生率可与肿瘤易感性窗口的宽度相关。仅存在狭窄窗口的例子包括髓上皮瘤、脑神经母细胞瘤、神经节胶质瘤和室管膜母细胞瘤等罕见肿瘤。相比之下,小脑髓母细胞瘤、星形细胞瘤、混合性星形细胞瘤和少突胶质细胞瘤以及胶质母细胞瘤则是根据细胞神经发生和胶质细胞出生后复制能力存在相对较宽易感性窗口的实例。胶质瘤的发生与脑损伤后或多发性硬化症时可能出现的细胞性胶质增生之间偶尔建立的关系也可以根据这一概念来看待。需要提高对放射后胶质瘤发生的认识,尤其是在急性淋巴细胞白血病明显成功治疗之后。

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