Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1522282 (EMT)
 2,868 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous injection of the gallium chelating agents, N,N'-ethylene bis[2-hydroxy-5-carboxyphenyl-glycine], (COOH-EHPG), or desferrioxamine (DFO) after gallium-67 (67Ga) injection, improved tumour/non-tumour tissue uptake ratios in mice bearing the EMT-6 sarcoma. Six hours post injection of gallium and 2 h post chelator, COOH-EHPG enhanced the tumour/blood ratios by an order of magnitude compared to untreated controls, whereas DFO increased the ratios three-fold. Twenty two hours post gallium and 2 h post chelator, the increases in ratios compared to controls were seven-fold for COOH-EHPG and two-fold for DFO. The study thus demonstrated the superior ability of COOH-EHPG for the enhancement of 67Ga tumour/blood ratios compared with DFO.
Int J Rad Appl Instrum B 1988
PMID:Chelator-induced enhancement of 67Ga tumour imaging: comparison of desferrioxamine with N,N'-ethylene-bis[2-hydroxy-5-carboxyphenylglycine]. 325 99

67Ga citrate and 99mTc citrate (Solcocitran) were injected sequentially, with an interval of 48 h, into Balb/c mice bearing transplanted EMT-6 tumors. Tissue distributions of 67Ga and 99mTc were measured simultaneously at intervals of 1, 3, 5 and 8 h after injection of the 99mTc citrate (49, 51, 53 and 56 h after 67Ga citrate). Maximal tumor:blood ratios for 67Ga and 99mTc were 13.8 +/- 3.2 and 4.0 +/- 1.0 respectively, both occurring at the final period. The maximum tumor index (T.I. = T:B X % dose/g) for 67Ga was 71 +/- 23% 56 h after injection, and for 99mTc was 13 +/- 12% 1 h after injection. Liver, kidney and spleen had equal or higher concentrations of radioactivity than tumor for either radiotracer. The somewhat higher tumor:blood ratio for 67Ga citrate was offset by the time required for this optimum to be reached. Alternatively, the best 99mTc citrate tumor:blood ratios were attained within 8 h, with less liver and gut radioactivity. These data fall within the range of results from other clinical and animal model studies of 67Ga citrate and 99mTc citrate. In view of the radiation dose, the inconvenience of the 48-72 h wait, and the cost of 67Ga, and because neither radiopharmaceutical is tumor specific, 99mTc citrate may have a place in early oncological screening. The results are discussed as part of a comprehensive review of the 99mTc citrate literature.
Int J Rad Appl Instrum B 1986
PMID:Comparative studies of radiocitrates in oncological models--I. 99mTc citrate and 67Ga citrate uptake by EMT-6 tumors in mice. 346 79

Glioblastoma multiforme (GBM) is an extremely aggressive brain cancer with a median survival of less than 2 years. GBM is characterized by abnormal activation of receptor tyrosine kinase and constitutively activated STAT3. Although EGFR phosphorylation and STAT3 activation are essential for the maintenance of GBM cancer stem cells, the molecular mechanism underlying endosome-mediated STAT3 activation is not fully understood. In the current study, we showed that GTP-binding protein RRAD (RAS associated with diabetes, RAD) physically associates with EGFR, and EEA1, enhancing the stability and endosome-associated nuclear translocation of EGFR. Functionally, RRAD contributes to the activation of STAT3 and expression of the stem cell factors OCT4, NANOG, and SOX2, thereby enhancing self-renewing ability, tumor sphere formation, EMT, and in vivo tumorigenesis. Most importantly, RRAD contributes to poor survival in patients with GBM. RRAD expression is correlated with temozolomide resistance, and, conversely, depletion of RRAD leads to sensitization of highly temozolomide-resistant GBM cells. Our data collectively support a novel function of RRAD in STAT3 activation and provide evidence that RRAD acts as a positive regulator in the EGFR signaling pathway. These results demonstrate a critical role for RRAD in GBM tumorigenesis and provide a rationale for the development of pharmacologic inhibitors of RRAD in GBM.
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PMID:RRAD promotes EGFR-mediated STAT3 activation and induces temozolomide resistance of malignant glioblastoma. 2531 11