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Life sciences · Journal article
Acta Haematologica Polonica · September 3, 2026
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EZH2, the catalytic subunit of PRC2, serves as a key epigenetic regulator of hematopoietic homeostasis. Its dysregulation — ranging from gain-of-function mutations in B-cell lymphomas to loss-of-function variants in myeloid neoplasms — drives oncogenesis through its complex dual role as both an oncogene and a tumor suppressor. This review provides a comprehensive synthesis of current knowledge on EZH2 structure, function, and the molecular mechanisms underlying its involvement in leukemias, lymphomas, and myelodysplastic syndromes. We highlight the role of NGS as an indispensable tool for baseline genomic profiling and accurate patient stratification at diagnosis. Furthermore, the review explores the evolving diagnostic landscape, emphasizing the transition toward ultrasensitive monitoring using liquid biopsy and ctDNA. The therapeutic landscape of EZH2-targeted approaches is critically assessed, including established therapies such as tazemetostat and dual EZH1/2 inhibitors, as well as emerging strategies such as PROTAC-mediated degradation and CRISPR-based gene editing. Finally, we address the challenges of acquired resistance and the urgent need for predictive biomarkers to optimize clinical outcomes. By integrating mechanistic insights with current clinical data, this review outlines a framework for personalized epigenetic care in hematology.