Analysis of the CDKI-73 (CDKI73) and fludarabine (FLUDARA)-regulated transcriptomes in human primary chronic lymphocytic leukemia (CLL) cells

2019 ◽  
Author(s):  
C Pepper
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Lymphocytic Leukemia ◽  
Primary Chronic Lymphocytic Leukemia

scholarly journals Interaction with Vascular Endothelium Enhances Survival in Primary Chronic Lymphocytic Leukemia Cells via NF-κB Activation and De novo Gene Transcription

2010 ◽  
Vol 70 (19) ◽  
pp. 7523-7533 ◽  
Author(s):  
Andrea G.S. Buggins ◽  
Chris Pepper ◽  
Piers E.M. Patten ◽  
Saman Hewamana ◽  
Satyen Gohil ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Gene Transcription ◽  
Vascular Endothelium ◽  
De Novo ◽  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
De Novo Gene ◽  
Primary Chronic Lymphocytic Leukemia

scholarly journals Chemoproteomics-based kinome profiling and target deconvolution of clinical multi-kinase inhibitors in primary chronic lymphocytic leukemia cells

Leukemia ◽  
2010 ◽  
Vol 25 (1) ◽  
pp. 89-100 ◽  
Author(s):  
U Kruse ◽  
C P Pallasch ◽  
M Bantscheff ◽  
D Eberhard ◽  
L Frenzel ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Kinase Inhibitors ◽  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
Target Deconvolution ◽  
Primary Chronic Lymphocytic Leukemia

Abstract 3207: Telomerase inhibition affects fludarabine sensitivity in quiescent primary chronic lymphocytic leukemia lymphocytes

2010 ◽  
Author(s):  
May Shawi ◽  
Lilian Amrein ◽  
Sergei Gryaznov ◽  
Chantal Autexier ◽  
Raquel Aloyz
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Lymphocytic Leukemia ◽  
Telomerase Inhibition ◽  
Primary Chronic Lymphocytic Leukemia

scholarly journals Genetic modification of primary chronic lymphocytic leukemia cells with a lentivirus expressing CD38

Haematologica ◽  
2010 ◽  
Vol 95 (3) ◽  
pp. 514-517 ◽  
Author(s):  
L. Pearce ◽  
L. Morgan ◽  
T. T. Lin ◽  
S. Hewamana ◽  
R. J. Matthews ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Genetic Modification ◽  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
Primary Chronic Lymphocytic Leukemia

scholarly journals Evaluation of bendamustine in combination with fludarabine in primary chronic lymphocytic leukemia cells

Blood ◽  
2014 ◽  
Vol 123 (24) ◽  
pp. 3780-3789 ◽  
Author(s):  
Amal A. El-Mabhouh ◽  
Mary L. Ayres ◽  
Elizabeth J. Shpall ◽  
Veerabhadran Baladandayuthapani ◽  
Michael J. Keating ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Dna Synthesis ◽  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
Unscheduled Dna Synthesis ◽  
Key Points ◽  
Primary Chronic Lymphocytic Leukemia

Key Points The fludarabine and bendamustine combination is cytotoxic to CLL cells even in the presence of a protective microenvironment. H2AX activation was maximum with the combination, and unscheduled DNA synthesis induced by bendamustine was blocked by fludarabine.

199 Targeting the apoptotic pathway with BCL-2 inhibitors sensitizes primary chronic lymphocytic leukemia to VSV-induced oncolysis

Cytokine ◽  
2008 ◽  
Vol 43 (3) ◽  
pp. 287
Author(s):  
Vanessa F. Tumilasci ◽  
Stephanie Oliere ◽  
John Bell ◽  
John Hiscott
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Lymphocytic Leukemia ◽  
Apoptotic Pathway ◽  
Primary Chronic Lymphocytic Leukemia

scholarly journals Rapid and efficient nonviral gene delivery of CD154 to primary chronic lymphocytic leukemia cells

2005 ◽  
Vol 13 (2) ◽  
pp. 215-224 ◽  
Author(s):  
L H Li ◽  
E Biagi ◽  
C Allen ◽  
R Shivakumar ◽  
J M Weiss ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Gene Delivery ◽  
Lymphocytic Leukemia ◽  
Nonviral Gene Delivery ◽  
Leukemia Cells ◽  
Primary Chronic Lymphocytic Leukemia

scholarly journals Docosahexaenoic acid induces apoptosis in primary chronic lymphocytic leukemia cells

2015 ◽  
Vol 7 (4) ◽  
Author(s):  
Romain Guièze ◽  
Emmanuel Gyan ◽  
Olivier Tournilhac ◽  
Christelle Halty ◽  
Richard Veyrat-Masson ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Docosahexaenoic Acid ◽  
Lymphocytic Leukemia ◽  
Dependent Manner ◽  
Omega 3 ◽  
Infectious Risk ◽  
Highly Active ◽  
Primary Chronic Lymphocytic Leukemia

Chronic lymphocytic leukemia is an indolent disorder with an increased infectious risk remaining one of the main causes of death. Development of therapies with higher safety profile is thus a challenging issue. Docosahexaenoic acid (DHA, 22:6) is an omega-3 fatty acid, a natural compound of normal cells, and has been shown to display antitumor potency in cancer. We evaluated the potential <em>in</em> <em>vitro</em> effect of DHA in primary CLL cells. DHA induces high level of <em>in</em> <em>vitro</em> apoptosis compared to oleic acid in a dose-dependent and time-dependent manner. Estimation of IC50 was only of 4.813 μM, which appears lower than those reported in solid cancers. DHA is highly active on CLL cells <em>in vitro.</em> This observation provides a rationale for further studies aiming to understand its mechanisms of action and its potent <em>in vivo</em> activity.

Proteasome Inhibiters Up-Regulate TRAIL/Apo2L and Its Receptors Significantly Contributing to Proteasome Inhibitor-Induced Apoptosis in Primary Chronic Lymphocytic Leukemia (CLL) Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2810-2810
Author(s):  
Albert F. Kabore ◽  
Kristin McCrea ◽  
James B. Johnston ◽  
Spencer B. Gibson
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Proteasome Inhibitor ◽  
Substantial Reduction ◽  
Proteasome Inhibitors ◽  
Lymphocytic Leukemia ◽  
Apoptotic Pathway ◽  
Protein Levels ◽  
Trail Receptors ◽  
Induced Apoptosis ◽  
Primary Chronic Lymphocytic Leukemia

Abstract The proteasome inhibitor, bortezomib has recently emerged as a new therapeutic treatment for refractory multiple myeloma and is presently being evaluated for other hematological malignancies either alone or in combination with other antitumor agents. Proteasome inhibitors cause the accumulation of many proteins but the precise mechanism responsible for their antitumor effect is unclear. In the present study, we have determined that cytotoxic effect the proteasome inhibitor MG-132 in primary chronic lymphocytic leukemia (CLL) cells is through the activation of the TRAIL (tumor necrosis factor-related apoptosis inducing ligand) apoptotic pathway. MG-132 induced apoptosis in approximately 70% of primary CLL cells as measured by annexin V staining. Addition of DR4:Fc that prevents TRAIL ligation with its receptors decreased the amount of MG-132 induced apoptosis by approximately 40% suggesting MG-132 caused activation of the TRAIL apoptotic pathway. MG-132 also up-regulated both the mRNA and protein levels of TRAIL and protein levels of TRAIL receptors DR4 and DR5. This upregulation correlated with activation of caspase 8 and cleavage of pro-apoptotic Bcl-2 family member Bid. Moreover, MG-132 treatment also induced a substantial reduction in the FLICE-like inhibitory protein (c-FLIP) protein levels. In contrast to CLL cells, proteasome inhibitors failed to activate the TRAIL apoptotic pathway in normal B-cells. This indicates that proteasome inhibitors are inducing apoptosis in primary CLL cells through activation of the TRAIL apoptotic signaling pathway through up-regulation of TRAIL and its cognate receptors and reduced FLIP expression. Thus, proteasome inhibitors may have a therapeutic role in CLL, either when used alone or in combination with TRAIL or antibodies against DR4/DR5.

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