Journal
FRONTIERS IN ONCOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.638288
Keywords
multiple myeloma; pathophysiology; lipoproteins; signaling; lipids; bone marrow; HDL
Categories
Funding
- European Union (European Social Fund-ESF) through the operational Program, Human Resources Development, Education and Lifelong Learning 2014-2020 [MIS 5047155]
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Multiple myeloma is an incurable hematologic disorder characterized by malignant plasma cells in the bone marrow. Lipid metabolism, obesity, and age are associated with the disease. Abnormal levels of lipids and lipoproteins have been reported in patients with MM, with higher APOA1 levels correlating to better survival outcomes. Deregulation of the lipoprotein transport system may facilitate disease development, and further analyses of serum lipoproteins could shed light on novel mechanisms of MM pathophysiology.
Multiple myeloma (MM) is an incurable neoplastic hematologic disorder characterized by malignant plasma cells, mainly in the bone marrow. MM is associated with multiple factors, such as lipid metabolism, obesity, and age-associated disease development. Although, the precise pathogenetic mechanisms remain unknown, abnormal lipid and lipoprotein levels have been reported in patients with MM. Interestingly, patients with higher APOA1 levels, the major apolipoprotein of high density lipoprotein (HDL), have better overall survival. The limited existing studies regarding serum lipoproteins in MM are inconclusive, and often contradictory. Nevertheless, it appears that deregulation of the lipoprotein transport system may facilitate the development of the disease. Here, we provide a critical review of the literature on the role of lipids and lipoproteins in MM pathophysiology. We also propose novel mechanisms, linking the development and progression of MM to the metabolism of blood lipoproteins. We anticipate that proteomic and lipidomic analyses of serum lipoproteins along with analyses of their functionality may improve our understanding and shed light on novel mechanistic aspects of MM pathophysiology.
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