3-4-5-trihydroxybenzamidoxime has been researched along with Precursor-Cell-Lymphoblastic-Leukemia-Lymphoma* in 2 studies
2 other study(ies) available for 3-4-5-trihydroxybenzamidoxime and Precursor-Cell-Lymphoblastic-Leukemia-Lymphoma
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Trimidox-induced apoptosis is mediated through induction of p53 in NALM-6 cells.
We examined the effect of trimidox-induced apoptosis involvement of p53 in the NALM-6 cell line of acute lymphoblastic leukemia. Trimidox has been shown to increase the induction of p53. Phosphorylation of p53 protein at Ser-15 and Ser-20 residues was activated earlier than the obvious increase in p53 expression. Pifithrin-alpha, a p53 inhibitor, significantly prevented trimidox-induced apoptotic characteristics, as detected by nuclear morphological observation and DNA fragmentation. Trimidox-induced apoptosis was enhanced or attenuated by transfection with wild-type or dominant-negative p53 containing expression vectors, respectively. These results indicate that one of the induction mechanisms of apoptosis by trimidox is the mediated augmentation of p53. Topics: Apoptosis; Benzamidines; Cell Line, Tumor; DNA Fragmentation; Enzyme Inhibitors; Humans; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Ribonucleotide Reductases; Signal Transduction; Tumor Suppressor Protein p53 | 2008 |
Interaction of gallium nitrate with other inhibitors of ribonucleotide reductase: effects on the proliferation of human leukemic cells.
Ribonucleotide reductase, a key enzyme in deoxyribonucleotide synthesis, is an important target for cancer chemotherapy. Drugs that inhibit its individual components may act synergistically to block DNA synthesis. Prior work has established that gallium inhibits the R2 subunit of ribonucleotide reductase. We show that gallium acts synergistically with the ribonucleotide reductase inhibitors gemcitabine and hydroxyurea to inhibit the proliferation of CCRF-CEM cells. In contrast, combinations of gallium with the ribonucleotide reductase inhibitors amidox, didox, or trimidox produced antagonistic effects on cell growth. Spectroscopy analysis revealed that as a result of their metal-binding properties, amidox, didox and trimidox formed complexes with gallium, thus negating potential synergistic actions. Our results have important implications in the design of clinical trials using these ribonucleotide reductase inhibitors in combination. Topics: Antineoplastic Agents; Benzamidines; Cell Division; Deoxycytidine; Drug Synergism; Enzyme Inhibitors; Gallium; Gemcitabine; Humans; Hydroxamic Acids; Hydroxyurea; Oximes; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Ribonucleotide Reductases; Tumor Cells, Cultured | 1998 |