| Literature DB >> 33418988 |
Stefania Stella1,2, Michele Massimino1,2, Livia Manzella1,2, Maria Stella Pennisi1,2, Elena Tirrò1,2, Chiara Romano1,2, Silvia Rita Vitale1,2, Adriana Puma1,2, Cristina Tomarchio1,2, Sandra Di Gregorio1,2, Giuseppe Alberto Palumbo3, Paolo Vigneri1,2.
Abstract
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.Entities:
Keywords: NGS; PDGFRα and PDGFRβ fusions; TCR rearrangements; hypereosinophilia; hypereosinophilic syndromes
Year: 2021 PMID: 33418988 DOI: 10.3390/ijms22020486
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923