Disturbed Plasma Lipidomic Profiles in Females with Diffuse Large B-Cell Lymphoma: A Pilot Study

Lipidome dysregulation is a hallmark of cancer and inflammation. The global plasma lipidome and sub-lipidome of inflammatory pathways have not been reported in diffuse large B-cell lymphoma (DLBCL). In a pilot study of plasma lipid variation in female DLBCL patients and BMI-matched disease-free cont...

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Bibliographic Details
Published in:Cancers 2023-07, Vol.15 (14), p.3653
Main Authors: Masnikosa, Romana, Pirić, David, Post, Julia Maria, Cvetković, Zorica, Petrović, Snježana, Paunović, Marija, Vučić, Vesna, Bindila, Laura
Format: Article
Language:English
Subjects:
Arachidonic acid
B cells
B-cell lymphoma
Biomarkers
Biopsy
Cancer
Cancer therapies
Cell membranes
Development and progression
Disease
Dyslipidemia
Eicosanoids
Females
Hematology
Immune system
Immunity
Immunocompetence
Inflammation
Ions
Lipid metabolism
Lipids
Lipoxygenase
Liquid chromatography
Lymphocytes B
Lymphoma
Malignancy
Mass spectrometry
Mass spectroscopy
Metabolism
Non-Hodgkin's lymphoma
Non-Hodgkin's lymphomas
Phosphatidylinositol
Physiological aspects
Pilot projects
Plasma
Signal transduction
Sphingolipids
Sphingosine
Sphingosine 1-phosphate
Type 2 diabetes
Unsaturated fatty acids
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Summary:Lipidome dysregulation is a hallmark of cancer and inflammation. The global plasma lipidome and sub-lipidome of inflammatory pathways have not been reported in diffuse large B-cell lymphoma (DLBCL). In a pilot study of plasma lipid variation in female DLBCL patients and BMI-matched disease-free controls, we performed targeted lipidomics using LC-MRM to quantify lipid mediators of inflammation and immunity, and those known or hypothesised to be involved in cancer progression: sphingolipids, resolvin D1, arachidonic acid (AA)-derived oxylipins, such as hydroxyeicosatetraenoic acids (HETEs) and dihydroxyeicosatrienoic acids, along with their membrane structural precursors. We report on the role of the eicosanoids in the separation of DLBCL from controls, along with lysophosphatidylinositol LPI 20:4, implying notable changes in lipid metabolic and/or signalling pathways, particularly pertaining to AA lipoxygenase pathway and glycerophospholipid remodelling in the cell membrane. We suggest here the set of S1P, SM 36:1, SM 34:1 and PI 34:1 as DLBCL lipid signatures which could serve as a basis for the prospective validation in larger DLBCL cohorts. Additionally, untargeted lipidomics indicates a substantial change in the overall lipid metabolism in DLBCL. The plasma lipid profiling of DLBCL patients helps to better understand the specific lipid dysregulations and pathways in this cancer.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers15143653