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2016 ; 57
(4
): 758-65
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Metabolism pathways in chronic lymphocytic leukemia
#MMPMID26643954
Rozovski U
; Hazan-Halevy I
; Barzilai M
; Keating MJ
; Estrov Z
Leuk Lymphoma
2016[]; 57
(4
): 758-65
PMID26643954
show ga
Alterations in chronic lymphocytic leukemia (CLL) cell metabolism have been
studied by several investigators. Unlike normal B lymphocytes or other leukemia
cells, CLL cells, like adipocytes, store lipids and utilize free fatty acids
(FFA) to produce chemical energy. None of the recently identified mutations in
CLL directly affects metabolic pathways, suggesting that genetic alterations do
not directly contribute to CLL cells' metabolic reprogramming. Conversely, recent
data suggest that activation of STAT3 or downregulation of microRNA-125 levels
plays a crucial role in the utilization of FFA to meet the CLL cells' metabolic
needs. STAT3, known to be constitutively activated in CLL, increases the levels
of lipoprotein lipase (LPL) that mediates lipoprotein uptake and shifts the CLL
cells' metabolism towards utilization of FFA. Herein, we review the evidence for
altered lipid metabolism, increased mitochondrial activity and formation of
reactive oxygen species (ROS) in CLL cells, and discuss the possible therapeutic
strategies to inhibit lipid metabolism pathways in patient with CLL.
|*Energy Metabolism/drug effects
[MESH]
|*Metabolic Networks and Pathways/drug effects
[MESH]
|Antineoplastic Agents/pharmacology/therapeutic use
[MESH]
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