Major
Neuroscience
Anticipated Graduation Year
2023
Access Type
Open Access
Abstract
Sustained remission of acute myeloid leukemia (AML) is negated by the proliferation of leukemia stem cells (LSCs) that survive first-line chemotherapy. Thus, there is a dire need for additional, LSC-specific therapies that can help prevent relapse. TBK1, a serine/ threonine kinase, has been implicated in the pathogenesis of AML, possibly due to its ability to promote MYC activity and FLT3 expression. Additionally, high TBK1 mRNA expression has been associated with a reduced probability of AML survival. We hypothesize that TBK1 inhibition could antagonize the stem-like characteristics of LSCs, promoting their loss-of-function death and increasing the odds of achieving a cure.
Community Partners
Department of Cancer Biology, Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center
Faculty Mentors & Instructors
Jiwang Zhang, MD, PhD; Austin P. Runde, MS Student in Cellular and Molecular Oncology; Fr. Peter Breslin, S.J.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.
Investigating the role of TANK-binding kinase 1 (TBK1) in MLL-AF9+ acute myeloid leukemia.
Sustained remission of acute myeloid leukemia (AML) is negated by the proliferation of leukemia stem cells (LSCs) that survive first-line chemotherapy. Thus, there is a dire need for additional, LSC-specific therapies that can help prevent relapse. TBK1, a serine/ threonine kinase, has been implicated in the pathogenesis of AML, possibly due to its ability to promote MYC activity and FLT3 expression. Additionally, high TBK1 mRNA expression has been associated with a reduced probability of AML survival. We hypothesize that TBK1 inhibition could antagonize the stem-like characteristics of LSCs, promoting their loss-of-function death and increasing the odds of achieving a cure.