dc.contributor.author | Constantinou, Andreas I. | en |
dc.contributor.author | Grdina, D. | en |
dc.contributor.author | Kiguchi, K. | en |
dc.contributor.author | Huberman, E. | en |
dc.creator | Constantinou, Andreas I. | en |
dc.creator | Grdina, D. | en |
dc.creator | Kiguchi, K. | en |
dc.creator | Huberman, E. | en |
dc.date.accessioned | 2019-11-04T12:50:21Z | |
dc.date.available | 2019-11-04T12:50:21Z | |
dc.date.issued | 1992 | |
dc.identifier.uri | http://gnosis.library.ucy.ac.cy/handle/7/52989 | |
dc.description.abstract | Treatment of human K-562-J leukemia cells for 1 h with the topoisomerase II-reactive drugs VP-16, VM-26, or mAMSA resulted in a dose-dependent inhibition of proliferation and in an increase in the percentage of cells staining positive for hemoglobin, a marker of erythroid differentiation. Staining for hemoglobin of up to about 60% of the cells was observed at 20 μM VP-16, 1 μM VM-26, and 8 μM mAMSA. Such treatment also caused a G2 M arrest in the cell cycle. Incubation of the cells with radiolabeled VP-16 indicated that the induced erythroid differentiation was not due to continuous cell exposure to a residual amount of the drug. VP-16-induced erythroid differentiation was also not affected by DNA, RNA, or protein synthesis inhibitors. Differentiation induction and the G2 M arrest evoked by VP-16, VM-26, and mAMSA were, however, reduced in the presence of novobiocin. Our results indicate that topo-reactive drugs that cause G2 M arrest in the K-562-J cell cycle can induce in these cells erythroid differentiation after a short and irreversible interaction with their target molecule(s). © 1992. | en |
dc.source | Experimental cell research | en |
dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026496572&doi=10.1016%2f0014-4827%2892%2990044-9&partnerID=40&md5=abfe2ab57a6bf6e6a6fa9d11835c0c65 | |
dc.subject | article | en |
dc.subject | etoposide | en |
dc.subject | human | en |
dc.subject | controlled study | en |
dc.subject | priority journal | en |
dc.subject | drug exposure | en |
dc.subject | dose response | en |
dc.subject | drug mechanism | en |
dc.subject | camptothecin | en |
dc.subject | human cell | en |
dc.subject | cell differentiation | en |
dc.subject | Kinetics | en |
dc.subject | cell growth | en |
dc.subject | cell cycle | en |
dc.subject | Hemoglobins | en |
dc.subject | Melanins | en |
dc.subject | Comparative Study | en |
dc.subject | teniposide | en |
dc.subject | amsacrine | en |
dc.subject | DNA Topoisomerases, Type II | en |
dc.subject | Support, U.S. Gov't, P.H.S. | en |
dc.subject | leukemia cell | en |
dc.subject | Tumor Cells, Cultured | en |
dc.subject | Dose-Response Relationship, Drug | en |
dc.subject | Aphidicolin | en |
dc.subject | cell cycle g2 phase | en |
dc.subject | cordycepin | en |
dc.subject | cycloheximide | en |
dc.subject | Deoxyadenosines | en |
dc.subject | dimethyl sulfoxide | en |
dc.subject | dna synthesis | en |
dc.subject | dna topoisomerase (atp hydrolysing) | en |
dc.subject | erythroid cell | en |
dc.subject | G2 Phase | en |
dc.subject | Leukemia, Myeloid, Chronic | en |
dc.subject | Mitosis | en |
dc.subject | novobiocin | en |
dc.subject | protein synthesis inhibition | en |
dc.subject | rna synthesis | en |
dc.subject | Support, U.S. Gov't, Non-P.H.S. | en |
dc.title | The effect of topoisomerase inhibitors on the expression of differentiation markers and cell cycle progression in human K-562 leukemia cells | en |
dc.type | info:eu-repo/semantics/article | |
dc.identifier.doi | 10.1016/0014-4827(92)90044-9 | |
dc.description.volume | 203 | |
dc.description.startingpage | 100 | |
dc.description.endingpage | 106 | |
dc.author.faculty | Σχολή Θετικών και Εφαρμοσμένων Επιστημών / Faculty of Pure and Applied Sciences | |
dc.author.department | Τμήμα Βιολογικών Επιστημών / Department of Biological Sciences | |
dc.type.uhtype | Article | en |
dc.description.notes | <p>Manufacturers: bristol | en |
dc.description.notes | national cancer institute | en |
dc.description.notes | sigma, United States | en |
dc.description.notes | Cited By :20</p> | en |
dc.source.abbreviation | Exp.Cell Res. | en |
dc.contributor.orcid | Constantinou, Andreas I. [0000-0003-0365-1821] | |
dc.gnosis.orcid | 0000-0003-0365-1821 | |