TCRF
Scientific Research

Patients with acute myeloid leukemia (AML) have a relatively poor outcome, compared with those with acute lymphocytic leukemia (ALL), another major type of leukemia. AML patients are associated with a high risk of disease come-back. Currently, immunotherapies, which mobilize a patient’s own T cells to eliminate cancer cells, have proven effective against other leukemias, particularly ALL. However, currently available immunotherapy approaches have been less effective against AML. Recently, several biology studies have shown that stimulating endogenous transposable elements, namely, long-interspersed-element-1 (L1), can induce a strong anti-tumor immune response. Herein, our preliminary study in an AML mouse model showed that antagonizing a novel enzyme can promote L1 and stimulation of the immune system, blocking disease development. Dr. Li proposes that this new drug could be developed as an anti-AML therapy and tested either alone or combined with other immunotherapies in future clinical trials.

This research’s focus is on how to increase the durability of cancer treatment responses and prevent the emergence of drug resistance; specifically identifying new therapeutic targets and approaches which eradicate minimal residual disease that persists in patients after initial treatment responses. This work has the potential to reveal new therapies which will transform transient responses into cures for patients.