Ionizing radiation (IR) is a standard-of-care treatment for glioma patients; however, the clinical efficacy is limited due to therapeutic resistance. A recent study published by Ma et al. (Cancer Cell 35:504–518, 2019) reported that the phosphorylation of phosphatase and tensin homolog (PTEN) at tyrosine 240 (pY240-PTEN) promotes the radioresistance of human glioma cells. After treatment with IR, the fibroblast growth factor receptor 2 (FGFR2)-mediated phosphorylation that generated pY240-PTEN could effectively promote the decondensation of chromatin through an interaction with Ki-67, leading to DNA damage repair and radioresistance. However, such promising findings need to be addressed in detail after considering the following points. (1) The authors should take into consideration whether or not the nuclear-cytoplasmic translocalization of PTEN occurs. (2) The roles of FGFR2-PTEN downregulation should be validated using both genetic and pharmacological inhibition models. (3) Some of the data shown by the authors are confusing and did not support the conclusion that patients with higher PTEN and FGFR2 expression were relatively IR resistant.

中文翻译：

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FGFR2介导的酪氨酸240上PTEN的磷酸化有助于神经胶质瘤的放射抵抗。

电离辐射（IR）是神经胶质瘤患者的标准治疗方法；然而，由于治疗抗性，临床疗效受到限制。Ma等发表的最新研究。（Cancer Cell 35：504–518，2019）报告说，酪氨酸240（pY240-PTEN）处的磷酸酶和张力蛋白同源物（PTEN）的磷酸化促进了人类神经胶质瘤细胞的放射抵抗力。经IR处理后，生成pY240-PTEN的成纤维细胞生长因子受体2（FGFR2）介导的磷酸化可通过与Ki-67相互作用而有效地促进染色质的解聚，从而导致DNA损伤修复和抗辐射性。但是，在考虑以下几点后，需要对这些有希望的发现进行详细处理。（1）作者应考虑是否发生了PTEN的核质转移。（2）FGFR2-PTEN下调的作用应通过遗传和药理学抑制模型来验证。（3）作者显示的一些数据令人困惑，并不支持PTEN和FGFR2表达较高的患者对IR耐药的结论。