ArticleJournal of neuro-oncology1990
A cerebral glioma model for experimental therapy and in vivo invasion studies in syngeneic BD IX rats.
Article in Journal of neuro-oncology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 31 citations in OpenAlex.
- Enhanced cytotoxic effects of 5-aminolevulinic acid-mediated photodynamic therapy by concurrent hyperthermia in glioma spheroids.Journal of neuro-oncology · 2004Article
- Interaction between microwave-induced brain hyperthermia and high dose rate radiation in the BT4 An brain glioma in rats.Journal of neuro-oncology · 1996Article
- Comparative aspects of neoplastic invasion of the brain.Journal of neuro-oncology · 1994Review
- Brain Tumor Working Group Report on the 9th International Conference on Brain Tumor Research and Therapy. Organ System Program, National Cancer Institute.Journal of neuro-oncology · 1993Article
- Combination of endostatin and a protein kinase Calpha DNA enzyme improves the survival of rats with malignant glioma.Neoplasia (New York, N.Y.)Article
- Models for assessment of angiogenesis in gliomas.Journal of neuro-oncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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