New target for potential leukemia therapy

The study provides both mechanistic and preclinical evidence supporting the rapid initiation of clinical trials for patients with acute myeloid leukemia to test an existing medicine that inhibits the complex, called eganelisib, both alone and in combination with the most used AML chemotherapy, cytarabine.

The Dana-Farber team took a different approach to searching for therapeutic targets. Rather than focusing on mutations, first author Qingyu Luo, MD, PhD, a research fellow in Lane's lab, used genome wide CRISPR interference to search for genes that AML cells rely on to grow.This hit was attractive in part because the PI3Kgamma complex had been studied before, though not in AML. In addition, a medicine already existed to inhibit it.

Looking at The Cancer Genome Atlas Data , the team found that patients with AML predicted to be sensitive to eganelisib don't do as well in terms of survival on existing therapies compared to those with negative biomarkers. This finding suggests that this patient group, which can be identified by high levels ofexpression, has a need for new medicines and could potentially benefit from treatment with eganelisib.

The observations suggested that the two medicines worked synergistically. Luo investigated and found that PI3Kgamma, when inhibited, also results in the suppression of a leukemia cell metabolic process called oxidative phosphorylation . Leukemia cells depend on OXPHOS for energy, and suppression of OXPHOS can result in their demise.

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