An in vivo
glioma model was developed in syngeneic BD IX rats. The BT4An
tumor was derived from serial in vivo passages of the BT4A
tumor, originally induced from transformed fetal rat brain cells after transplacental exposure to
ethylnitrosourea. The cell line was characterized for the presence of neuroglial
differentiation markers, chromosome content and cell cycle distribution as determined by flowcytometry. A standardized method for i.c.
tumor induction was developed, and the
tumors were investigated by light and electron microscopy and for evidence of blood-brain barrier disruption.
Tumor cell ability for phagocytosis was studied, as this property may be important for the invasion pattern of the
tumors. We conclude that the model seems suitable for both in vivo
therapy and invasion studies. The
tumor had 100%
tumor take, yielded a predictable symptom-free life span after inoculation, had a characteristic histological picture of an aggressive
glioma, and the blood-brain barrier within the
tumor was in part disrupted. Compared to the parent cell line, there was loss of neuroglial
differentiation markers, the chromosomal distribution was changed, and the ability for phagocytosis was practically lost.