Leukemia Research Foundation funds UC study targeting RhoA in TP53-mutated AML
核心洞察
The Leukemia Research Foundation (搜索) has awarded funding to a University of Cincinnati study investigating RhoA (搜索) as a therapeutic target in TP53-mutated acute myeloid leukemia (搜索) (AML).
Patients with TP53-mutated leukemia often respond poorly to available treatments, with survival typically measured in months, underscoring an urgent unmet need.
Preliminary research identified RhoA (搜索) as a potential key driver of drug resistance in TP53-mutant AML, and it can be blocked with experimental drugs.
Patients with TP53-mutated leukemia often do not respond well to the treatments that are currently available, with survival usually measured in months. This poor prognosis underscores the urgent need for new therapeutic strategies, and a newly funded study at the University of Cincinnati aims to address it by targeting a protein called RhoA (搜索).
The Leukemia Research Foundation (搜索) has awarded grant funding to Skuli, assistant professor in the UC College of Medicine and a Cancer Center physician, to investigate RhoA (搜索) as a potential therapeutic vulnerability in TP53-mutated acute myeloid leukemia (搜索) (AML).
Skuli's previous research found that TP53-mutant AML cells rely on a specific metabolic pathway that produces molecules that help activate proteins the cancer cells need to grow and survive. Building on this work, preliminary studies identified RhoA (搜索) as a potential key driver of drug resistance in TP53-mutant AML.
"In preliminary studies, I identified one of these proteins, called RhoA (搜索), as a potential key driver of drug resistance in TP53-mutant AML," said Skuli. "Importantly, RhoA can be blocked with experimental drugs, making it a promising new treatment target."
Supported by the grant funding, Skuli will test whether blocking RhoA (搜索) makes TP53-mutant AML cells more sensitive to these AML therapies using cell and animal models and patient-donated samples.
"If successful, this project will identify RhoA (搜索) as a new therapeutic vulnerability of TP53-mutant AML and provide the preclinical evidence needed to support future clinical trials testing RhoA-targeted strategies," Skuli said.