Titles + affiliations
Assistant Professor, Cancer Epigenetics Program
Fox Chase Cancer Center
Targeting LSD1 in Senescence-Like Resilient AML Cells
Despite many advances in AML therapy and initial response to treatment, most patients will eventually relapse and succumb to the disease. There is a significant need to better understand the mechanisms that enable relapse of AML for developing novel therapeutic interventions. We recently discovered that AML cells enter a senescence-like state in response to chemotherapy. This process facilitates survival of AML cells by allowing them to endure chemotherapy in a transiently dormant state while retaining the potential to repopulate leukemia. It is important to target these senescence-like dormant AML cells as they represent a pool of leukemia cells capable of initiating relapse. Hence, it is critical to identify key factors and understand the biology underlying the senescence-like leukemia cells. We identified a role of LSD1 in the senescence-like cells and will determine the functional consequence of LSD1 deficiency. Completion of this proposal will contribute to a better understanding of mechanisms regulating the senescence-like resilient phenotype in AML, which can provide a basis for future therapeutic interventions.
The Leukemia Research Foundation grant allowed my recently launched laboratory to pursue innovative research towards understanding therapy-induced senescent-like leukemia cells that are capable of initiating leukemia relapse. Findings from this grant, together with new collaborations established during this project, are instrumental to pursue novel therapeutic approaches against senescence-like leukemia cells and provide the foundation for new research angles and grant applications.
Leukemia Research Foundation grant
$100K awarded in 2021
Acute myeloid leukemia (AML)
Cancer cell biology (leukemia cell biology)