Kroh H, Cervós-Navarro J
Acta Neuropathol. 1983;59(4):309-15. doi: 10.1007/BF00691498.
The aim of this EM study was to assess the relationship of demyelination changes induced in mouse brain by a carcinogenic substance to the early steps in the evolution of neoplastic disease. The investigation on the 25 experimental mice injected at various stages of age with ethylnitrosourea revealed demyelination foci in three animals and interfascicular nests of abnormal cells in seven animals, the latter most probably being of oligodendroglial origin. The nest cells were characterized by their large size and a multitude of interdigitated cytoplasmic processes forming complicated membranous patterns. The abnormal development of oligodendroglial cytoplasmic processes is considered to be the cause of the demyelination. This previously unknown form of oligodendroglial transformation may consist in either the earliest preneoplastic changes or represent a reactive, paraneoplastic type of alteration.
本电子显微镜研究的目的是评估致癌物质在小鼠大脑中诱导的脱髓鞘变化与肿瘤性疾病演变早期阶段的关系。对25只在不同年龄阶段注射乙基亚硝基脲的实验小鼠进行的调查显示,三只动物出现了脱髓鞘病灶,七只动物出现了束间异常细胞巢,后者很可能起源于少突胶质细胞。巢细胞的特征是体积大,有大量相互交错的细胞质突起,形成复杂的膜状结构。少突胶质细胞质突起的异常发育被认为是脱髓鞘的原因。这种以前未知的少突胶质细胞转化形式可能要么是最早的肿瘤前变化,要么代表一种反应性、副肿瘤性改变类型。