Molecular Pathogenesis and Treatment Perspectives for Hypereosinophilia and Hypereosinophilic Syndromes.
Stefania StellaMichele MassiminoLivia ManzellaMaria Stella PennisiElena TirròChiara RomanoSilvia Rita VitaleAdriana PumaCristina TomarchioSandra Di GregorioGiuseppe Alberto Maria PalumboPaolo VigneriPublished in: International journal of molecular sciences (2021)
Hypereosinophilia (HE) is a heterogeneous condition with a persistent elevated eosinophil count of >350/mm3, which is reported in various (inflammatory, allergic, infectious, or neoplastic) diseases with distinct pathophysiological pathways. HE may be associated with tissue or organ damage and, in this case, the disorder is classified as hypereosinophilic syndrome (HES). Different studies have allowed for the discovery of two major pathogenetic variants known as myeloid or lymphocytic HES. With the advent of molecular genetic analyses, such as T-cell receptor gene rearrangement assays and Next Generation Sequencing, it is possible to better characterize these syndromes and establish which patients will benefit from pharmacological targeted therapy. In this review, we highlight the molecular alterations that are involved in the pathogenesis of eosinophil disorders and revise possible therapeutic approaches, either implemented in clinical practice or currently under investigation in clinical trials.
Keyphrases
- copy number
- clinical trial
- clinical practice
- end stage renal disease
- high throughput
- genome wide
- chronic kidney disease
- ejection fraction
- newly diagnosed
- single molecule
- randomized controlled trial
- dendritic cells
- patient reported outcomes
- immune response
- gene expression
- dna methylation
- single cell
- study protocol
- phase iii
- allergic rhinitis
- circulating tumor