Glucose and Methionine Uptake by Rat Brain Tumor Treated with Prodrug-Activated Gene Therapy

The effect of aciclovir (ACV) on the metabolism of rat 9L-gliosarcoma cells expressing the herpes simplex virus-thymidine kinase gene was studied using 2-deoxy-2-[ 18F]fluoro- d-glucose (FDG) and l-[methyl- 11C]methionine. Though the average weight of the tumors treated with ACV was significantly lo...

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Veröffentlicht in:	Nuclear medicine and biology 1998-04, Vol.25 (3), p.247-250
Hauptverfasser:	Namba, Hiroki, Iwadate, Yasuo, Iyo, Masaomi, Fukushi, Kiyoshi, Irie, Toshiaki, Sueyoshi, Kanji, Tagawa, Masatoshi, Sakiyama, Shigeru
Format:	Artikel
Sprache:	eng
Schlagworte:	Acyclovir - therapeutic use Animals Antiviral Agents - therapeutic use Biological and medical sciences Biological Transport Brain Neoplasms - metabolism Brain Neoplasms - pathology Brain Neoplasms - therapy Brain tumor Carbon Radioisotopes - pharmacokinetics Fluorodeoxyglucose Fluorodeoxyglucose F18 - pharmacokinetics Gene therapy Genetic Therapy Gliosarcoma - metabolism Gliosarcoma - pathology Gliosarcoma - therapy Glucose - metabolism Male Medical sciences Methionine Methionine - metabolism Neurology Prodrugs - therapeutic use Radiopharmaceuticals - pharmacokinetics Rats Rats, Inbred F344 Simplexvirus - enzymology Simplexvirus - genetics Thymidine Kinase - biosynthesis Thymidine Kinase - genetics Thymidine kinase gene Tumor metabolism Tumors of the nervous system. Phacomatoses
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Zusammenfassung:	The effect of aciclovir (ACV) on the metabolism of rat 9L-gliosarcoma cells expressing the herpes simplex virus-thymidine kinase gene was studied using 2-deoxy-2-[ 18F]fluoro- d-glucose (FDG) and l-[methyl- 11C]methionine. Though the average weight of the tumors treated with ACV was significantly lower than that of the saline-injected control group, FDG and methionine uptake per weight of tumor tissue was not different between the two groups. This result exhibits a striking contrast to the metabolic pattern observed after radiation therapy, suggesting the different pathways regarding tumor cell death between the therapies.
ISSN:	0969-8051 1872-9614
DOI:	10.1016/S0969-8051(97)00171-6