Detailed characterization of the mouse glioma 261 tumor model for experimental glioblastoma therapy
Detailed characterization of the mouse glioma 261 tumor model for experimental glioblastoma therapy
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DOI：
10.1111/j.1349-7006.2006.00208.x
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发表时间：
2006-06-01
期刊：
影响因子：
5.7
通讯作者：
Safrany, Geza
中科院分区：
文献类型：
--
作者：
Szatmari, Tunde;Lumniczky, Katalin;Safrany, Geza
小鼠神经胶质瘤261（G1261）细胞经常用于实验性胶质母细胞瘤治疗;然而，G1261肿瘤模型的详细描述不可用。在这里，我们提出，G1261细胞携带点突变的K-ras和p53基因。基础的主要组织相容性复合体（MHC）I，但不是MHCII，在G1261细胞中检测到的表达。干扰素γ编码基因的引入增加了MHCI和MHCII的表达。在野生型细胞中检测到少量的B7-1和B7-2 RNA，但细胞因子的产生并没有改变表达水平。腺病毒载体可有效转导G1261细胞，逆转录病毒载体的感染性有限。少量移植的Gl 261细胞在C57 BL/6小鼠中形成皮下和颅内肿瘤。这些细胞具有中等免疫原性：在颅内肿瘤攻击前7天用经照射的肿瘤细胞预接种小鼠可预防约90%的小鼠肿瘤形成。当在肿瘤攻击后的第一天或第三天进行疫苗接种时，没有发现存活的动物。体外生长的细胞是放射敏感的：达到50%的细胞死亡率需要小于2戈伊。用4戈伊X射线对脑肿瘤荷瘤小鼠进行局部肿瘤照射可减缓肿瘤进展，但没有一只小鼠的肿瘤被治愈。总之，Gl 261脑肿瘤模型可有效地用于研究各种治疗方式的抗肿瘤作用，但应考虑细胞的中等免疫原性。
Mouse glioma 261 (Gl261) cells are used frequently in experimental glioblastoma therapy; however, no detailed description of the Gl261 tumor model is available. Here we present that Gl261 cells carry point mutations in the K-ras and p53 genes. Basal major histocompatibility complex (MHC)I, but not MHCII, expression was detected in Gl261 cells. The introduction of interferon-gamma-encoding genes increased expression of both MHCI and MHCII. A low amount of B7-1 and B7-2 RNA was detected in wild-type cells, but cytokine production did not change expression levels. Gl261 cells were transduced efficiently by adenoviral vectors; the infectivity of retroviral vectors was limited. Low numbers of transplanted Gl261 cells formed both subcutaneous and intracranial tumors in C57BL/6 mice. The cells were moderately immunogenic: prevaccination of mice with irradiated tumor cells 7 days before intracranial tumor challenge prevented tumor formation in approximately 90% of mice. When vaccination was carried out on the day or 3 days after tumor challenge, no surviving animals could be found. In vitro-growing cells were radiosensitive: less than 2 Gy was required to achieve 50% cell mortality. Local tumor irradiation with 4 Gy X-rays in brain tumor-bearing mice slowed down tumor progression, but none of the mice were cured off the tumor. In conclusion, the Gl261 brain tumor model might be efficiently used to study the antitumor effects of various therapeutic modalities, but the moderate immunogenicity of the cells should be considered.