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It highlights key therapeutic updates and identifies research gaps guiding future translation into practice.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/molecular-pathogenesis-and-targeted-therapies-for-myeloproliferative-hypereosinophilic-neoplasms/356454/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/molecular-pathogenesis-and-targeted-therapies-for-myeloproliferative-hypereosinophilic-neoplasms/356454.png","ImageObject",300,407,{"name":42,"@type":43},"River Wang","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-23","2026-09-23",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",6,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"What is the purpose of this review on myeloproliferative hypereosinophilic neoplasms?","Question",{"text":63,"@type":64},"The review synthesizes current understanding of molecular drivers and evaluates established and novel targeted therapies. It aims to deliver a clinically relevant update on how molecular precision changes diagnosis and management beyond imatinib.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"Which therapy remains standard for PDGFRA/B-rearranged disease, and why?",{"text":68,"@type":64},"Imatinib remains the standard for PDGFRA/B-rearranged disease. Resistance has led to next-generation inhibitors, reflecting the central role of specific molecular alterations.",{"name":70,"@type":61,"acceptedAnswer":71},"What major recent treatment and trial directions are highlighted?",{"text":72,"@type":64},"The review notes approval of pemigatinib for FGFR1-rearranged neoplasms, and it discusses defining roles of JAK inhibitors for JAK2-driven disease. It also describes ongoing exploration of monoclonal antibodies such as mepolizumab and benralizumab for symptom control in broader eosinophilic populations.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},356454,1790894818,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,105,109,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":55,"doc_module":4,"doc_module_name":25,"category_name":102,"show_sort_weight":103,"slug":104},"Technology",50,"technology",{"id":106,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":107,"slug":108},7,40,"healthcare",{"id":110,"doc_module":4,"doc_module_name":25,"category_name":111,"show_sort_weight":112,"slug":113},8,"Research & Report",30,"research-report",{"id":115,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},9,"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},19,"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":106,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":139,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":112},1099514067438,"https://ap-avatar.wpscdn.com/avatar/100002539ee87300030?x-image-process=image/resize,m_fixed,w_180,h_180&k=1780474512215547542","Current Hematologic Malignancy Reports (2026) 21:8  \n[https://doi.org/10.1007/s1](https://doi.org/10.1007/s1) 1899-026-00775-4  \nREVIEW  \nMolecular Pathogenesis and Targeted Therapies for Myeloproliferative Hypereosinophilic Neoplasms  \nColette Hanna1 · Joe Rizkallah2 · Nicole Charbel3 · Shereen Sakkal4 · Fadi G. Haddad5  \nReceived: 1 December 2025 / Accepted: 2 February 2026 © The Author(s) 2026  \nAbstract  \nPurpose of Review This review examines the rapidly evolving landscape of myeloproliferative hypereosinophilic syndromes (HES) and related neoplasms. We aim to synthesize current understanding of their diverse molecular drivers, evaluate the efficacy of established and novel targeted therapies, and identify critical research gaps. The goal is to provide a clinically relevant update on how molecular precision is reshaping the diagnosis and management of these rare, often aggressive hematologic malignancies beyond the established standard ofimatinib.  \nRecent Findings The field has moved beyond generic HES diagnoses to a molecularly defined classification. While imatinib remains the standard for PDGFRA/B-rearranged disease, resistance has spurred the development of next-generation inhibitors like avapritinib, which effectively targets the highly resistant PDGFRA D842V mutation. A major recent advance is the approval of pemigatinib for FGFR1-rearranged neoplasms, a historically chemo-refractory subgroup with a dismal prognosis. Clinical trials are also defining the roles of JAK inhibitors for JAK2-driven disease and exploring monoclonal antibodies like mepolizumab and benralizumab for symptom control in broader eosinophilic populations.  \nSummary The management of myeloproliferative HES has transitioned from empirical therapy to a precision medicine paradigm. Early comprehensive molecular profiling is essential to guide therapy selection. While imatinib remains a cornerstone for select patients, novel agents like pemigatinib and avapritinib have filled critical therapeutic gaps. Future progress depends on the routine integration of comprehensive next-generation sequencing, the validation of minimal residual disease monitoring to guide therapy de-escalation, and international collaboration to conduct innovative trials for these rare patient populations.  \nKeywords Hypereosinophilic syndrome · Myeloid/Lymphoid neoplasms with eosinophilia · FGFR1 rearrangement · FIP1L1-PDGFRA · Tyrosine kinase inhibitors  \nColette Hanna and Joe Rizkallah contributed equally to this work.  \n􀀍 Fadi G. Haddad[fhaddad@mdanderson.org](fhaddad@mdanderson.org)  \n1 Division of Hematology/Oncology, Lebanese American University Medical Center-Rizk Hospital, Beirut, Lebanon  \n2 Department of Diagnostic Radiology, American University of Beirut, Beirut, Lebanon  \n3 Division of Hematology and Oncology, Department of Internal Medicine, American University of Beirut, Beirut, Lebanon  \n4 Faculty of Medicine, University of Montreal, Montreal, Quebec, Canada  \n5 Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA  \nIntroduction  \nHypereosinophilic syndromes (HES) represent a heterogeneous group of disorders characterized by the core features of persistent and significant peripheral blood eosinophilia, defined as an absolute eosinophil count of 1.5 × 10⁹/L or greater [1, 2] . The clinical manifestations of HES are diverse, reflecting the potential of eosinophils to infiltrate and damage tissues. Patients may present with constitutional symptoms, dermatologic findings, pulmonary infiltrates, gastrointestinal distress, or, most ominously, life-threatening cardiac complications such as endomyocardial fibrosis and thromboembolism [1, 3] .  \nFor decades, the majority of HES cases lacking a clear secondary cause were classified as “idiopathic,” leaving clinicians with limited, non-specific therapeutic options,  \n1 3  \nprimarily corticosteroids and cytotoxic agents, which carried significant toxicity and offered variable efficacy [2","cbCaikE9qMDEkd3x","https://ap.wps.com/l/cbCaikE9qMDEkd3x","pdf",1169352,12,"English","# Abstract\n## Purpose of Review\n## Recent Findings\n## Summary\n# Introduction","[{\"question\":\"What is the purpose of this review on myeloproliferative hypereosinophilic neoplasms?\",\"answer\":\"The review synthesizes current understanding of molecular drivers and evaluates established and novel targeted therapies. It aims to deliver a clinically relevant update on how molecular precision changes diagnosis and management beyond imatinib.\"},{\"question\":\"Which therapy remains standard for PDGFRA/B-rearranged disease, and why?\",\"answer\":\"Imatinib remains the standard for PDGFRA/B-rearranged disease. Resistance has led to next-generation inhibitors, reflecting the central role of specific molecular alterations.\"},{\"question\":\"What major recent treatment and trial directions are highlighted?\",\"answer\":\"The review notes approval of pemigatinib for FGFR1-rearranged neoplasms, and it discusses defining roles of JAK inhibitors for JAK2-driven disease. It also describes ongoing exploration of monoclonal antibodies such as mepolizumab and benralizumab for symptom control in broader eosinophilic populations.\"}]","Molecular Pathogenesis and Targeted Therapies for Myeloproliferative Hypereosinophilic Neoplasms | PDF",1790125381]