Effect of deoxycytidine on the in vitro response of human leukemia cells to inhibitors of de novo pyrimidine biosynthesis

1987 ◽  
Vol 19 (3) ◽  
Author(s):  
Kapil Bhalla ◽  
Steven Grant
Keyword(s):  
De Novo ◽  
Pyrimidine Biosynthesis ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
In Vitro Response

scholarly journals The Effect of Autologous Serum on Lymphocyte Response to Human Leukemia Cells

Blood ◽  
1974 ◽  
Vol 43 (6) ◽  
pp. 781-787 ◽  
Author(s):  
J. Hugh Bryan ◽  
Gloria E. Johnson ◽  
Brigid G. Leventhal
Keyword(s):  
Leukemia Cells ◽  
Autologous Serum ◽  
Human Leukemia ◽  
Autologous Tumor ◽  
Lymphocyte Response ◽  
Tumor Bearing ◽  
Human Leukemia Cells ◽  
Blastogenic Response ◽  
In Vitro Response

Abstract The normal lymphocytes of 11 of 18 patients with acute leukemia in remission showed a positive blastogenic response in vitro to autologous leukemia cells. The effect of autologous serum on this response was studied to determine if there were factors which might abrogate or "block" this response. Serum obtained at diagnosis (i.e., during a tumor-bearing period) was compared with remission serum with the expectation of demonstrating a "blocking" effect of the former and no effect or perhaps even facilitation with the latter. However, this was not the case, and no consistent differences in blastogenesis in the presence of the two sera were seen. In addition, during the period of observation, there was little correlation between the presence or absence of in vitro response to autologous tumor and prognosis.

In Vitro Anti-proliferative Effects on NB4 Human Leukemia Cells and Physicochemical Screening of Pleurotus sp. (Higher Basidiomycetes) Mycelia from Cuba

2014 ◽  
Vol 16 (3) ◽  
pp. 239-245 ◽  
Author(s):  
Humberto J. Morris ◽  
Edgar Hernandez ◽  
Gabriel Llaurado ◽  
Maria Cristina Tejedor ◽  
Pilar Sancho ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells

Induction of lymphokine-activated killer cells against human leukemia cells in vitro

1989 ◽  
Vol 59 (1) ◽  
pp. 21-24 ◽  
Author(s):  
J. V. Teichmann ◽  
W. -D. Ludwig ◽  
H. Seibt-Jung ◽  
E. Thiel
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Lymphokine Activated Killer Cells ◽  
Killer Cells ◽  
Human Leukemia Cells

scholarly journals In Vitro and In Vivo Apoptosis-Inducing Antileukemic Effects of Mucuna macrocarpa Stem Extract on HL-60 Human Leukemia Cells

2010 ◽  
Vol 9 (3) ◽  
pp. 298-308 ◽  
Author(s):  
Kuan-Hung Lu ◽  
Yuh-Fang Chang ◽  
Pen-Hui Yin ◽  
Ting-Ting Chen ◽  
Yu-Ling Ho ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Stem Extract

Antiproliferative effects of some novel synthetic solanidine analogs on HL-60 human leukemia cells in vitro

Steroids ◽  
2011 ◽  
Vol 76 (1-2) ◽  
pp. 156-162 ◽  
Author(s):  
Renáta Minorics ◽  
Thomas Szekeres ◽  
Georg Krupitza ◽  
Philipp Saiko ◽  
Benedikt Giessrigl ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Antiproliferative Effects ◽  
Human Leukemia Cells

Enhanced therapeutic effects on the multi-drug resistant human leukemia cells in vitro and xenograft in mice using the stealthy liposomal vincristine plus quinacrine

2008 ◽  
Vol 22 (4) ◽  
pp. 429-437 ◽  
Author(s):  
Gong-Wen Liang ◽  
Wan-Liang Lu ◽  
Jin-Wei Wu ◽  
Ji-Hui Zhao ◽  
Hai-Yan Hong ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Therapeutic Effects ◽  
Human Leukemia ◽  
Drug Resistant ◽  
Human Leukemia Cells

scholarly journals Non-toxic polymer nanovectors for improved delivery of dexamethasone

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Benjamin C. Ede ◽  
Paraskevi Diamanti ◽  
David S. Williams ◽  
Allison Blair
Keyword(s):  
Drug Exposure ◽  
Free Drug ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Front Line ◽  
Broad Distribution ◽  
Human Leukemia Cells ◽  
Line Drug

AbstractDexamethasone (Dex) is a highly insoluble front-line drug used in cancer therapy. Data from clinical trials indicates that the pharmacokinetics of Dex vary considerably between patients and prolonging drug exposure rather than increasing absolute dose may improve efficacy. Non-toxic, fully biodegradable Dex loaded nanovectors (NV) were formulated, via simple direct hydration within 10 min, as a vehicle to extend exposure and distribution in vivo. Dex-NV were just as effective as the free drug against primary human leukemia cells in vitro and in vivo. Importantly, high levels of DMSO solvent were not required in the NV formulations. Broad distribution of NV was seen rapidly following inoculation into mice. NV accumulated in major organs, including bone marrow and brain, known sanctuary sites for ALL. The study describes a non-toxic, more easily scalable system for improving Dex solubility for use in cancer and can be applied to other medical conditions associated with inflammation.

scholarly journals Differential Incorporation of Ara-C, Gemcitabine, and Fludarabine Into Replicating and Repairing DNA in Proliferating Human Leukemia Cells

Blood ◽  
1997 ◽  
Vol 90 (1) ◽  
pp. 270-278 ◽  
Author(s):  
Hiromichi Iwasaki ◽  
Peng Huang ◽  
Michael J. Keating ◽  
William Plunkett
Keyword(s):  
Dna Repair ◽  
Ribonucleotide Reductase ◽  
De Novo ◽  
Gradient Centrifugation ◽  
Nucleoside Analogs ◽  
Repair Process ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Repair Synthesis ◽  
Human Leukemia Cells

The major actions of nucleoside analogs such as arabinosylcytosine (ara-C) and fludarabine occurs after their incorporation into DNA, during either replication or repair synthesis. The metabolic salvage and DNA incorporation of the normal nucleoside, deoxycytidine, is functionally compartmentalized toward repair synthesis in a process regulated by ribonucleotide reductase. The aim of this study was to investigate the metabolic pathways by which nucleoside analogs that do (fludarabine, gemcitabine) or do not (ara-C) affect ribonucleotide reductase are incorporated into DNA in proliferating human leukemia cells. Using alkaline density-gradient centrifugation to separate repaired DNA from replicating DNA and unreplicated parental DNA strands, approximately 60% of ara-C nucleotide in DNA was incorporated by repair synthesis in CCRF-CEM cells; the remainder was incorporated by replication. In contrast, fludarabine and gemcitabine, nucleosides that inhibit ribonucleotide reductase and decreased deoxynucleotide pools, were incorporated mainly within replicating DNA. Hydroxyurea also depleted deoxynucleotide pools and increased the incorporation of ara-C into DNA by replicative synthesis. Stimulation of DNA repair activity by UV irradiation selectively enhanced the incorporation of all nucleosides tested through repair synthesis. These findings suggest that the pathways by which therapeutically useful nucleoside analogs are incorporated into DNA are affected by cellular dNTP pools from de novo synthesis and by the relative activities of DNA repair and replication. The antitumor activity of these drugs may be enhanced by combination with either ribonucleotide reductase inhibitors to increase their incorporation into replicating DNA or with agents that induce DNA damage and evoke the DNA repair process.

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