Scientists from Tsinghua University and The Rockefeller University have identified a promising new pathway for treating acute myeloid leukemia (AML) by targeting the interaction between two key proteins: JMJD1C and RUNX1. Published in the journal Protein & Cell, the research reveals how these proteins collaborate to sustain leukemia cell survival, potentially opening a novel therapeutic approach.
AML is characterized by its genetic complexity and aggressive nature, making comprehensive treatment challenging. The study demonstrates that JMJD1C forms liquid-like molecular condensates when recruited by RUNX1 to specific genomic locations, activating genes critical for leukemia cell proliferation and metabolic processes.
The researchers discovered that disrupting JMJD1C's structural capabilities significantly reduces leukemia cell viability. By targeting the JMJD1C-RUNX1 axis, scientists hope to develop a more universal strategy that could potentially overcome the disease's notorious heterogeneity and resistance to current treatments.
Dr. Mo Chen, a senior study author, emphasized the significance of these findings, suggesting they could transform understanding of leukemia biology. The research provides a foundational approach to potentially develop therapies that could work across multiple AML subtypes, addressing a critical gap in current treatment strategies.
This breakthrough represents a significant step toward developing more effective, comprehensive treatments for one of the most challenging blood cancers. By focusing on the molecular mechanisms that sustain leukemia cells, researchers are moving closer to developing targeted interventions that could improve patient outcomes.
