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The process of blood cell formation is called hematopoiesis. Hematopoiesis starts early during development, on the seventh day of embryogenesis. This phase of hematopoiesis is called the primitive wave, wherein the extraembryonic yolk sac allows the production of erythroid cells and endothelial cells from a common precursor called hemangioblast. The erythroid cells provide oxygen to support the growth of the rapidly dividing embryo. Hemangioblasts later develop into hematopoietic stem cells or...

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Related Experiment Video

Updated: May 7, 2026

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

Published on: January 20, 2019

EZH2 in normal and malignant hematopoiesis.

K Lund¹, P D Adams², M Copland³

¹Department of Epigenetics of Cancer and Aging, Institute of Cancer Sciences, University of Glasgow, Cancer Research UK Beatson Labs, Glasgow, Scotland, UK.

|October 8, 2013

Summary

Enhancer of Zeste Homologue 2 (EZH2) plays a key role in blood stem cell development and cancer. Inhibiting EZH2 may treat lymphoma and leukemia, but its tumor-suppressor functions must be preserved.

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A Comprehensive Pipeline to Assess the Efficiency of Human Erythropoiesis In Vitro and Ex Vivo

A Comprehensive Pipeline to Assess the Efficiency of Human Erythropoiesis In Vitro and Ex Vivo

Published on: January 10, 2025

Area of Science:

Molecular Biology
Epigenetics
Hematology

Background:

Enhancer of Zeste Homologue 2 (EZH2) is a histone methyltransferase crucial for stem cell development and hematopoiesis.
EZH2 deposits H3K27me3, a mark associated with transcriptional repression, influencing cell fate.
Aberrant EZH2 expression is linked to tumorigenesis and cancer stem cell (CSC) states.

Purpose of the Study:

To review the complex role of EZH2 in normal and malignant hematopoiesis.
To discuss the therapeutic potential of EZH2 inhibition in hematological malignancies.
To highlight the challenges in targeting EZH2, balancing oncogenic and tumor-suppressor functions.

Main Methods:

Literature review of EZH2's function in hematopoiesis.
Analysis of EZH2's role in hematological malignancies (lymphoma, leukemia).
Examination of EZH2 inhibitors and therapeutic strategies.

Main Results:

EZH2 has a dual role in hematological malignancies, acting as both an oncogene and tumor suppressor.
Gain-of-function mutations in EZH2 are implicated in lymphoma, while inactivating mutations occur in leukemia.
EZH2 inhibition shows promise for reducing CSC self-renewal in lymphoma and leukemia.

Conclusions:

Targeting EZH2 offers a potential therapeutic strategy for hematological cancers.
Careful consideration of EZH2's dual role is necessary to avoid interfering with its tumor-suppressor functions.
Further research into specific EZH2 inhibitors is crucial for effective cancer therapy.