New Investigator Research Grant Program

Acute myeloid leukemia (AML) is an aggressive blood cancer with poor outcomes, especially in patients carrying mutations in a gene called TP53. While new immune-based treatments have been successful in other cancers, they often do not work well in TP53-mutant AML. Our research has uncovered a new reason why: not only do the leukemia cells carry TP53 mutations, but the patient’s own immune cells—specifically T cells—can also acquire these mutations. As a result, these T cells become “exhausted” and lose their ability to attack cancer effectively. This project will investigate how TP53 mutations disrupt T-cell function by altering gene regulation and damaging mitochondria, the energy-producing structures inside cells. We will also test whether restoring mitochondrial function can help these immune cells recover their activity. By understanding and reversing this dysfunction, our work aims to develop new strategies to improve immune therapies for patients with TP53-mutant AML and related blood cancers.