Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of chemotherapy on living tumor tissue in hamsters and rats were investigated by measuring the 31P nuclear magnetic resonance spectra using topical magnetic resonance. Human neuroblastoma, human glioblastoma, and rat glioma tumor cells were inoculated s.c. in the lumbar region of the animals. After the diameter of the tumors increased to 1.5 cm, in vivo 31P nuclear magnetic resonance spectra were measured selectively in the tumors with a TMR-32 spectrometer. Adenosine triphosphate, inorganic phosphate (Pi), phosphodiester, and phosphomonoester peaks were observed. The phosphocreatine peak was hardly detectable, adenosine triphosphate and phosphomonoester peaks were high, and tissue pH, calculated from the chemical shift of Pi, declined. Regardless of the tumor origin or the histological type, the spectral pattern of each neuroectodermal tumor was found to be essentially the same. After i.v. injection of a large dose of a chemotherapeutic agent, adenosine triphosphate peaks decreased and Pi increased gradually, resulting in a dominant Pi peak pattern after 6 to 12 hours. However, during the same period, there were no observable changes in the spectra of normal organs. These findings indicated that the drugs have a selective and direct action on the energy metabolism of tumor cells. With lower drug doses, no remarkable changes were seen in the spectrum. Measurement of in vivo 31P nuclear magnetic resonance spectra is valuable not only to investigate the energy metabolism in tumor tissue but also to evaluate the effects of chemotherapy.
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PMID:Measurements of in vivo 31P nuclear magnetic resonance spectra in neuroectodermal tumors for the evaluation of the effects of chemotherapy. 398 84

Radiation-induced gene expression was examined in cells of a radioresistant human glioblastoma cell line, T98G, using RNA fingerprinting by arbitrary primer polymerase chain reaction. Three of the differentially induced transcripts were cloned and identified as the mitochondrially encoded cytochrome c oxidase (MTCO) subunits 1 and 2, and NADH dehydrogenase subunit 4. The levels of all three mRNAs were increased 1 h after irradiation, with elevated expression persisting for at least 24 h. Similar to radiation, other oxidants lead to induction of MTCO1, an effect which could be prevented by the antioxidant pyrrolidine dithiocarbamate. These results indicate that the increase in mitochondrial gene expression is mediated by oxidative stress. Mitochondria could be a target of signaling by ionizing radiation and oxidants since it is known to be at the site of cellular oxidative stress. The proteins encoded by MTCO1 and other mitochondrial mRNAs characterized are part of the mitochondrial respiratory chain which produces adenosine triphosphate through the process of oxidative phosphorylation. Adenosine triphosphate levels and the mitochondrial membrane potential were found to be increased significantly after irradiation, while mitochondrial mass and mitochondrial DNA levels were unaffected. These data demonstrate the specificity of changes in mitochondrial activity and gene expression after irradiation.
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PMID:Ionizing radiation stimulates mitochondrial gene expression and activity. 980 91