Max Duer
Pronouns: He/Him
Research Mentor(s): Terrence Wong
Research Mentor School/College/Department: Internal Medicine / Medicine
Program: UROPF
Session: Session 6 (3:40pm – 4:30pm)
Authors: Max Duer, Terrence Wong
Abstract
Acute myeloid leukemia (AML) is a type of cancer that develops as a result of mutations in hematopoietic stem cells (HSCs). These mutations often lead to a faulty response to DNA damage, and recurrent mutations in the SRCAP gene have been identified in AML patients. SRCAP is a gene that plays a role in epigenetics by swapping the H2A histone for the H2A.Z variant. However, the precise mechanism by which mutations in SRCAP and disruption of this epigenetic pathway contribute to the development of AML is currently unknown. Our lab has previously found that the loss of SRCAP leads to increased DNA damage in HSCs in mice, and we believe that this loss may cause defective DNA repair, leading to more mutations and the development of leukemia. To understand how loss of SRCAP affects the response to DNA damage in HSCs, we will use a mouse model and hematopoietic cell lines to study the impact of loss of SRCAP in normal and leukemic cells. We hypothesize that the loss of SRCAP will result in decreased H2A.Z genome deposition and an increase in DNA damage at specific genomic locations. To test this, we will use a combination of H2A.Z and ?-H2A.X ChIP-seq techniques to study how loss of SRCAP affects the distribution of H2A.Z and DNA damage. By understanding how SRCAP loss impacts the response to DNA damage in HSCs, we hope to improve our understanding of how HSCs develop into leukemia and lead to more effective treatments for this disease.
