Researchers Uncover Potential New Treatment Strategy for Acute Myeloid Leukemia
TL;DR
Identified mechanism in AML treatment offers strategic advantage by targeting JMJD1C-RUNX1 axis, potentially overcoming disease heterogeneity.
JMJD1C forms liquid-like condensates with RUNX1, activating key genes for AML cell survival by regulating gene expression.
Research on JMJD1C's role in AML presents new therapeutic strategy, aiming to improve patient outcomes and tackle disease heterogeneity.
Study reveals JMJD1C's unique function in leukemia biology by forming condensates, shedding light on potential new treatments for AML.
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Researchers from Tsinghua University and The Rockefeller University have discovered a critical molecular mechanism that could transform the treatment of acute myeloid leukemia (AML). The study, published in Protein & Cell, identifies the protein JMJD1C as a key player in leukemia cell survival, potentially opening new pathways for therapeutic intervention.
AML is a complex and aggressive cancer characterized by uncontrolled growth of immature blood cells. Traditional treatments have struggled to address the disease's genetic diversity, often targeting specific genetic abnormalities while failing to disrupt the underlying transcriptional networks that sustain leukemia.
The research reveals that JMJD1C forms liquid-like molecular condensates when recruited by RUNX1 to specific genomic locations. These interactions activate genes crucial for AML cell proliferation and metabolic processes. Critically, the study demonstrates that disrupting JMJD1C's molecular structure can reduce leukemia cell viability.
Dr. Mo Chen, a senior author of the study, emphasized the significance of the findings, suggesting that targeting the JMJD1C-RUNX1 interaction could provide a universal strategy for treating AML across its various genetic subtypes. This approach could potentially overcome current limitations in treatment and improve patient outcomes.
The discovery represents a significant advancement in understanding leukemia's molecular mechanisms. By focusing on the non-catalytic functions of JMJD1C and its ability to form molecular condensates, researchers have identified a promising new therapeutic target that could revolutionize AML treatment.
Curated from 24-7 Press Release
