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

Simple Summary: Diffuse large B-cell lymphoma (DLBCL) is the predominant type of non-Hodgkin lymphoma—the most common haematological malignancy worldwide. These two cancers are cancers of the immune system and dyslipidemia is a hallmark of both cancer and inflammation. Cancer needs specific lipid species to sustain growth and survival. The global plasma lipidome and sub-lipidome of inflammatory pathways in DLBCL have not yet been reported. In order to address this gap, we conducted targeted lipidomics using liquid chromatography—multiple reaction monitoring to investigate bioactive plasma lipids involved in metabolic and signalling pathways of inflammation and immunity. The global lipidome change in plasma DLBCL was determined by four-dimensional trapped ion mobility mass spectrometry-based lipidomics. In our study, we observed differential lipid profiles in treatment-naïve female patients with DLBCL and disease-free controls. We suggest here the set of sphingosine 1-phosphate, sphingomyelins SM 36:1 and SM 34:1, and phosphatidylinositol PI 34:1 as DLBCL lipid signature, which could serve as a basis for the prospective validation in larger DLBCL cohorts. 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. [ABSTRACT FROM AUTHOR]