Disturbed Plasma Lipidomic Profiles in Females with Diffuse Large B-Cell Lymphoma: A Pilot Study
Author:
Masnikosa Romana1ORCID, Pirić David1, Post Julia Maria2, Cvetković Zorica34ORCID, Petrović Snježana5, Paunović Marija5ORCID, Vučić Vesna5ORCID, Bindila Laura2ORCID
Affiliation:
1. Department of Physical Chemistry, Vinca Institute of Nuclear Sciences—National Institute of the Republic of Serbia, University of Belgrade, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia 2. Clinical Lipidomics Unit, Institute of Physiological Chemistry, University Medical Centre of the J.G.U Mainz, Duesbergweg 6, 55128 Mainz, Germany 3. Department of Haematology, Clinical Hospital Centre Zemun, Vukova 9, 11000 Belgrade, Serbia 4. Faculty of Medicine, University of Belgrade, Dr. Subotića 8, 11000 Belgrade, Serbia 5. Group for Nutritional Biochemistry and Dietology, Centre of Research Excellence in Nutrition and Metabolism, Institute for Medical Research, National Institute of the Republic of Serbia, University of Belgrade, Tadeusa Koscuska 1, 11000 Belgrade, Serbia
Abstract
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.
Funder
Clinical Lipidomics Unit’s Core Facility at the Institute of Physiological Chemistry, University Medical Centre Mainz Germany Research Society Ministry of Education, Science and Technological Development of the Republic of Serbia BMBF-funded DIASyM
Subject
Cancer Research,Oncology
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