The role of key biomarkers in lymphatic malformation: An updated review

Abstract

The lymphatic system, crucial for tissue fluid balance and immune surveillance, can be severely impacted by disorders that hinder its activities. Lymphatic malformations (LMs) are caused by fluid accumulation in tissues owing to defects in lymphatic channel formation, the obstruction of lymphatic vessels or injury to lymphatic tissues. Somatic mutations, varying in symptoms based on lesions' location and size, provide insights into their molecular pathogenesis by identifying LMs' genetic causes. In this review, we collected the most recent findings about the role of genetic and inflammatory biomarkers in LMs that control the formation of these malformations. A thorough evaluation of the literature from 2000 to the present was conducted using the PubMed and Google Scholar databases. Although it is obvious that the vascular endothelial growth factor receptor 3 mutation accounts for a significant proportion of LM patients, several mutations in other genes thought to be linked to LM have also been discovered. Also, inflammatory mediators like interleukin‐6, interleukin‐8, tumor necrosis factor‐alpha and mammalian target of rapamycin are the most commonly associated biomarkers with LM. Understanding the mutations and genes expression responsible for the abnormalities in lymphatic endothelial cells could lead to novel therapeutic strategies based on molecular pathways.

Pro-inflammatory responses after peptide-based cancer immunotherapy

“…The innate immune system's antigen-presenting cells (APCs) are activated by the adaptive immune system. They are responsible for binding antigen to the major histocompatibility complex (MHC) and delivering it to the cell surface so that T cell receptors can recognize it [ [5] , [6] , [7] , [8] ]. MHC class I and II molecules interact by cytosolic intracellular peptides.…”