Journal ArticleDOI
Apoptosis as a mechanism of cell death induced by different chemotherapeutic drugs in human leukemic T-lymphocytes☆
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TLDR
No determinant role for Ca2+ in triggering the process of endonucleolytic cleavage of genomic DNA in these leukemic T-lymphocytes is suggested and a causal relationship between increasedCa2+i and induction of apoptosis could not be clearly established.About:
This article is published in Biochemical Pharmacology.The article was published on 1996-05-17. It has received 73 citations till now. The article focuses on the topics: Apoptosis & DNA fragmentation.read more
Citations
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Mechanisms of action of methotrexate.
Journal ArticleDOI
Oxythiamine and dehydroepiandrosterone induce a G1 phase cycle arrest in Ehrlich's tumor cells through inhibition of the pentose cycle.
Badr Raı̈s,Begoña Comin,Joaquim Puigjaner,J.L. Brandes,Edmond E. Creppy,Dominique Saboureau,R. Ennamany,Wai-Nang Paul Lee,Laszlo G. Boros,Marta Cascante +9 more
TL;DR: It is demonstrated that pentose cycle (PC) inhibitors, OT and dehydroepiandrosterone (DHEA), efficiently regulate the cell cycle and tumor proliferation processes and introduce a new target site for the development of future cancer therapies to inhibit glucose utilizing pathways selectively for nucleic acid production.
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The anti-inflammatory actions of methotrexate are critically dependent upon the production of reactive oxygen species.
TL;DR: ROS generation by MTX is important for cytostasis in monocytes and cytotoxicity T‐cells, and its clinical efficacy can be attributed to multiple targets.
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A novel apoptosis-like pathway, independent of mitochondria and caspases, induced by curcumin in human lymphoblastoid T (Jurkat) cells.
Katarzyna Piwocka,Krzysztof Zabłocki,Mariusz R. Wieckowski,Janusz Skierski,Izabella Feiga,Jan Szopa,Nadzieja Drela,Lech Wojtczak,Ewa Sikora +8 more
TL;DR: It is concluded that the programmed cell death induced by curcumin in Jurkat cells differs from "classical" by the lack of mitochondrial depolarization and of the involvement of caspases.
Journal Article
A nuclear protein complex containing high mobility group proteins B1 and B2, heat shock cognate protein 70, ERp60, and glyceraldehyde-3-phosphate dehydrogenase is involved in the cytotoxic response to DNA modified by incorporation of anticancer nucleoside analogues.
TL;DR: Findings indicate that the HMGB1-HMGB2-HSC70-ERp60-glyceraldehyde 3-phosphate dehydrogenase complex detects changes in DNA structure caused by incorporation of nonnatural nucleosides and is a determinant of cell sensitivity to such DNA modifying chemotherapy.
References
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A new generation of Ca2+ indicators with greatly improved fluorescence properties.
TL;DR: A new family of highly fluorescent indicators has been synthesized for biochemical studies of the physiological role of cytosolic free Ca2+ using an 8-coordinate tetracarboxylate chelating site with stilbene chromophores that offer up to 30-fold brighter fluorescence.
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Apoptosis. The role of the endonuclease
TL;DR: In apoptosis, selective activation of an endogenous endonuclease appears to be responsible not only for widespread chromatin cleavage but also for the major nuclear morphologic changes, including conservation of the nucleolin-rich fibrillar center.
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Apoptotic death in epithelial cells: cleavage of DNA to 300 and/or 50 kb fragments prior to or in the absence of internucleosomal fragmentation.
F. Oberhammer,J.W. Wilson,Caroline Dive,I.D. Morris,John A. Hickman,A.E. Wakeling,P.R. Walker,M. Sikorska +7 more
TL;DR: Results suggest that changes in the integrity of DNA indicative of the release of chromatin loop domains occur before cleavage at internucleosomal sites is initiated and that the latter is not an essential step in the apoptotic process.
Journal Article
Induction of Endonucleolytic DNA Cleavage in Human Acute Myelogenous Leukemia Cells by Etoposide, Camptothecin, and Other Cytotoxic Anticancer Drugs: A Cautionary Note
TL;DR: The results suggest that endonucleolytic DNA damage by a preexisting cellular enzyme occurs soon after treatment of HL-60 cells with any of a variety of cytotoxic agents, and calls into question the selectivity of the degradative process for DNA.
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Activation of programmed cell death (apoptosis) by cisplatin, other anticancer drugs, toxins and hyperthermia.
TL;DR: Analysis of cell death induced by cisplatin in Chinese hamster ovary cell lines suggests that, irrespective of the primary site of action of a drug, cell death by most pharmacologic agents is mediated by activation of the signal transduction pathway for apoptosis.