New Vulnerability in Aggressive Leukemia Discovered by Researchers

Excerpt from the Press Release:

A potential weakness in a common form of leukemia could lead to new treatments. The discovery, made by researchers at the Lewis Katz School of Medicine at Temple University, shows that leukemia cells with mutations in DNMT3A—a gene often altered in acute myeloid leukemia (AML)—depend on a DNA-repair enzyme known as DNA polymerase theta (Polθ) to survive. Targeting this enzyme could lead to novel ways to fight aggressive leukemia.

The research, published in Cell Reports Medicine, is the first to show that DNMT3A-mutant leukemia cells become highly dependent on Polθ, leaving them vulnerable to attack by selective therapeutic agents. 

“DNMT3A mutations are common in AML but leukemia cells carrying these mutations have been difficult to eliminate,” said senior investigator Tomasz Skorski, MD, PhD, DSc, Director of the Fels Cancer Institute for Personalized Medicine and Professor in the Department of Cancer and Cellular Biology at the Lewis Katz School of Medicine and co-leader of the Nuclear Dynamics and Cancer Program at the Fox Chase Cancer Center. “By uncovering the dependency on Polθ, we have identified a new weakness that could be exploited therapeutically.” 

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