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Abstract：
It is essential to seek the underlying molecular mechanisms of glioma development, and critical to discover interventions that reduce the incidence and attenuate the growth of gliomas using a well-established in vivo experimental model because glioma is clinically one of the most difficult malignant tumors to treat. Ethylnitrosourea (ENU)-induced glioma in the rat has been extensively utilized as an experimental brain tumor model since the mid-1960s, however, the scientific value of ENU-induced glioma has been underappreciated mainly due to the recent development of transgenic mouse glioma models. Because of the pathophysiological characteristics, which are similar to the high grade human malignant gliomas, ENU-induced glioma is an excellent in vivo model to: a) examine the cell origin, development, and pathophysiology of gliomas; b) investigate anti-tumor effects of calorie restriction (CR) and its underlying mechanisms; and c) discover new preventive and/or therapeutic interventions of glioma. Further exploration of genetic changes during initiation, malignant transformation of glial cells, and progression of glioma as well as CR\'s anti-tumor effects on cellular processes using cutting edge technology, e.g., spatial transcriptomics, could provide more insight and a deeper understanding of the pathophysiology of gliomas.
摘要：
寻求神经胶质瘤发展的潜在分子机制至关重要，并且使用建立良好的体内实验模型来发现降低神经胶质瘤发病率和减轻神经胶质瘤生长的干预措施至关重要，因为神经胶质瘤是临床上最难治疗的恶性肿瘤之一。自1960年代中期以来，乙基亚硝基脲（ENU）诱导的大鼠神经胶质瘤已被广泛用作实验性脑肿瘤模型，然而,ENU诱导的神经胶质瘤的科学价值被低估,这主要是由于最近发展了转基因小鼠神经胶质瘤模型.由于病理生理的特点,类似于高级人类恶性胶质瘤，ENU诱导的神经胶质瘤是一种极好的体内模型：a)检查细胞起源，发展,和神经胶质瘤的病理生理学;b)研究热量限制(CR)的抗肿瘤作用及其潜在机制;和c)发现神经胶质瘤的新的预防和/或治疗干预措施。在启动过程中进一步探索遗传变化，胶质细胞的恶性转化，和胶质瘤的进展以及CR对细胞过程的抗肿瘤作用，使用尖端技术，例如，空间转录组学，可以提供更多的见解和更深入的了解神经胶质瘤的病理生理学。
