Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 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

Adenosine triphosphate (ATP) regulates surfactant phospholipid secretion from alveolar type II cells by interacting with P2-purinoceptors on the alveolar type II cell surface. To further characterize regulation of surfactant secretion, we have cloned the type II cell P2u-purinoceptor and expressed a functional receptor in an unrelated cell line. The coding sequence of the P2u clone isolated from a type II cell cDNA library was 1.1 kb, encoding a putative protein of 374 amino acids. The putative protein demonstrated > 97% homology with the P2u-purinoceptor previously identified in the hybrid neuroblastoma x glioma cell line, NG 108-15, 87% homology to the recently cloned human P2u-purinoceptor, and 34% homology to the P2u-purinoceptor cloned from chicken brain. The putative type II cell P2u protein contains seven membrane-spanning domains, characteristic of G-protein-coupled receptors. The type II cell P2u-purinoceptor nucleotide sequence also demonstrated > 95% homology to the nucleotide sequence of the NG 108-15 clone. However, the type II cell cDNA also demonstrated presence of an additional 208 bp insert in the 5' untranslated region, which was not present in the NG 108-15 clone. Using reverse transcriptase polymerase chain reaction, we examined expression of the two different sizes of mRNA in various rat tissues. Only the larger type II cell mRNA was expressed in rat heart, kidney, lung, spleen, and testis, with no expression of P2u-purinoceptor mRNA noted in brain or liver. The smaller species of mRNA was only detected in mouse N18-TG2 cells, and these cells expressed a larger species as well, found in the rat tissues noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cloning and expression of the alveolar type II cell P2u-purinergic receptor. 781 68

Macrophages are involved in cancer progression. M1 macrophages have an antitumor effect, whereas M2 phenotype are associated with tumor growth. The progression of gliomas involves the participation of an inflammatory microenvironment. Adenosine triphosphate (ATP) can act as pro-inflammatory signal, whereas adenosine has opposite properties. The biological effects of extracellular nucleotides/nucleosides mediated by purinergic receptors are controlled by ectonucleotidases. In the present work, we evaluated whether glioma-conditioned medium (GL-CM) modulates macrophage differentiation and the participation of ATP and adenosine in the release of pro-and anti-inflammatory cytokines by these cells. The results show that macrophages exposed to GL-CM were modulated to an M2-like phenotype. HPLC analysis of GL-CM demonstrated the presence of significant amounts of ATP and its metabolites. Macrophages exposed to GL-CM presented decreased ATP and AMP hydrolysis and increased IL-10 and MCP-1 secretion, effects that were diminished by P1 or P2 antagonists. GL-CM did not alter the release of IL-6 by macrophages, although treatment with ATP promoted an increase in the release of IL-6, which was prevented by a P2X7 antagonist. In summary, we found that A2A and P2X7 activation is necessary for IL-10, MCP-1, and IL-6 release by macrophages exposed to GL-CM, which, in turn, modulates the macrophages to M2-phenotype. The present study establishes a relationship between M2-like polarization, cytokine release and purinergic receptor activation in macrophages exposed to GL-CM. Therefore, the data presented herein contributes to advancing in the field of cancer-related inflammation and point specific purinergic receptors as targets for modulation of the phenotype of glioma-associated macrophages.
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PMID:Involvement of purinergic system in the release of cytokines by macrophages exposed to glioma-conditioned medium. 2554 98