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Updated: Nov 10, 2025
Investigation of Genetic Dependencies Using CRISPR-Cas9-based Competition Assays
Published on: January 7, 2019
Targeting differentiation blockade in AML: New hope from cell-surface-based CRISPR screens
Rui Su1, Ying Qing2, Jianjun Chen3
1Department of Systems Biology, Beckman Research Institute of City of Hope, Monrovia, CA 91016, USA.
Researchers identified ZFP36L2 as a key regulator of myeloid leukemia cell differentiation. Targeting this regulator offers a promising new therapeutic strategy for acute myeloid leukemia (AML).
Area of Science:
- Hematology
- Cancer Biology
- Molecular Biology
Background:
- Acute myeloid leukemia (AML) is characterized by the accumulation of undifferentiated myeloid progenitors.
- Targeting the differentiation blockade in AML presents a viable therapeutic strategy.
Purpose of the Study:
- To identify novel regulators of myeloid differentiation in AML.
- To explore ZFP36L2 as a potential therapeutic target for AML.
Main Methods:
- Surface antigen-guided CRISPR screening was employed.
- Functional assays were performed to assess ZFP36L2's role in myeloid differentiation.
Main Results:
- ZFP36L2 was identified as a crucial regulator of myeloid differentiation in AML.
- The study highlights ZFP36L2 as a potential therapeutic target.
Conclusions:
- ZFP36L2 plays a significant role in controlling myeloid differentiation in AML.
- Targeting ZFP36L2 may offer a new avenue for AML treatment.
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