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Related Experiment Video

Updated: May 14, 2026

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Published on: May 17, 2024

Eosinophilic myeloid neoplasms.

Pierre Noel¹, Ruben A Mesa

¹Division of Hematology Oncology, Mayo Clinic Arizona, Scottsdale, Arizona 85259, USA. Noel.Pierre@Mayo.edu

Current Opinion in Hematology

|February 7, 2013

Summary

Idiopathic hypereosinophilic syndrome (HES) remains a diagnosis of exclusion. Identifying imatinib-responsive fusion proteins in eosinophilic myeloproliferative neoplasms (MPNs) improves diagnosis and targeted therapy for persistent eosinophilia.

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Database-guided Flow-cytometry for Evaluation of Bone Marrow Myeloid Cell Maturation

Database-guided Flow-cytometry for Evaluation of Bone Marrow Myeloid Cell Maturation

Published on: November 3, 2018

Area of Science:

Hematology
Oncology
Molecular Biology

Background:

Idiopathic hypereosinophilic syndrome (HES) is a diagnosis of exclusion for persistent eosinophilia.
Eosinophilic myeloid neoplasms (MPNs) are increasingly recognized, challenging the diagnosis of HES.
Accurate diagnosis of eosinophilic MPNs remains low, estimated at 10-20% of persistent primary hypereosinophilia cases.

Purpose of the Study:

To review recent advancements in diagnosing and treating eosinophilic myeloid neoplasms.
To highlight the impact of identifying specific fusion proteins on patient management.
To discuss the ongoing challenges in differentiating HES from other eosinophilic disorders.

Main Methods:

Review of the World Health Organization (WHO) classification of hypereosinophilic MPNs.
Analysis of diagnostic criteria and molecular targets for eosinophilic disorders.
Synthesis of current research on pathophysiology and therapeutic strategies.

Main Results:

The WHO established a semi-molecular classification for hypereosinophilic MPNs in 2008.
Discovery of PDGFRA, PDGFRB, FGFR1, JAK-2, and FLT3 fusion proteins enables targeted therapies.
Patients with PDGFRA and PDGFRB fusion genes show responsiveness to imatinib therapy.

Conclusions:

Continued research is crucial for understanding eosinophilia pathophysiology and refining diagnostic boundaries.
Identifying novel therapeutic targets is essential to reduce the number of HES diagnoses.
Advances in molecular diagnostics are transforming the approach to eosinophilic neoplasms.