J Neurosci：科学家发现不同的脑瘤或存在相同的起源

  神经胶质瘤是一种常见的恶性脑瘤，不同类型的神经胶质瘤通常作为不同的疾病来诊断，而且其被认为是由大脑中不同的细胞类型所引发的；如今来自乌普萨拉大学等处的研究人员通过研究揭示，不同类型的脑瘤或许起源于同一种细胞，该研究发现或可帮助揭示不同脑瘤形成的分子机制，为开发治疗特殊神经胶质瘤的新型靶向疗法提供新的希望。
  相关研究刊登于国际杂志Journal of Neuroscience上；最常见的神经胶质瘤为星形细胞瘤和少突神经胶质瘤，后者被认为是由寡突细胞而引发，星形细胞瘤患者预后往往比少突神经胶质瘤患者预后差，而这两种肿瘤在临床上是被分开诊断的。
  研究者Lene Uhrbom表示，尽管不同种类型肿瘤看似不同而且其存在不同的预后结果，而且有研究推测其或许起源于大脑中不同类型的细胞，但实际上精确的细胞起源并不确定。研究者一直致力于寻找神经胶质瘤的细胞起源及引发肿瘤的遗传改变。
  这项研究中，研究人员利用患神经胶质瘤的小鼠进行研究，利用星形细胞瘤和少突神经胶质瘤肿瘤模型进行实验，研究者就发现这两个非常相似的肿瘤均起源于同一种名为少突胶质前体细胞的细胞，少突胶质前体细胞可以产生上述两种脑部肿瘤。
  研究者发现，并不是细胞起源而是遗传畸变控制着肿瘤类型的形成，通过分析大量人类星形细胞瘤和少突神经胶质瘤的基因活性，研究者表示，许多不同类型的肿瘤比我们之前想象中要相似地多，如今我们就可以看到，此前被认为只能形成少突神经胶质瘤的细胞类型同样也可以形成星形细胞瘤，这项最新研究为揭示引发神经细胞瘤的基础分子机制也提供了新的思路和线索。（转化医学网360zhyx.com）
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Oncogenic Signaling Is Dominant to Cell of Origin and Dictates Astrocytic or Oligodendroglial Tumor Development from Oligodendrocyte Precursor Cells
The Journal of Neuroscience doi: 10.1523/JNEUROSCI.2977-14.2014
Nanna Lindberg1,2,3, Yiwen Jiang1,*, Yuan Xie1,*, Hamid Bolouri3, Marianne Kastemar1, Tommie Olofsson4, Eric C. Holland2,3,5, and Lene Uhrbom1
Stem cells, believed to be the cellular origin of glioma, are able to generate gliomas, according to experimental studies. Here we investigated the potential and circumstances of more differentiated cells to generate glioma development. We and others have shown that oligodendrocyte precursor cells (OPCs) can also be the cell of origin for experimental oligodendroglial tumors. However, the question of whether OPCs have the capacity to initiate astrocytic gliomas remains unanswered. Astrocytic and oligodendroglial tumors represent the two most common groups of glioma and have been considered as distinct disease groups with putatively different origins. Here we show that mouse OPCs can give rise to both types of glioma given the right circumstances. We analyzed tumors induced by K-RAS and AKT and compared them to oligodendroglial platelet-derived growth factor B-induced tumors in Ctv-a mice with targeted deletions of Cdkn2a (p16Ink4a−/−, p19Arf−/−, Cdkn2a−/−). Our results showed that glioma can originate from OPCs through overexpression of K-RAS and AKT when combined with p19Arf loss, and these tumors displayed an astrocytic histology and high expression of astrocytic markers. We argue that OPCs have the potential to develop both astrocytic and oligodendroglial tumors given loss of p19Arf, and that oncogenic signaling is dominant to cell of origin in determining glioma phenotype. Our mouse data are supported by the fact that human astrocytoma and oligodendroglioma display a high degree of overlap in global gene expression with no clear distinctions between the two diagnoses.