Katerndahl Lab

The laboratory of Casey Katerndahl, Ph.D., seeks to identify the molecular mechanisms that regulate the pathogenesis of Acute Myeloid Leukemia.

Approximately 20,000 adult patients develop acute myeloid leukemia (AML) each year; these patients have a ~25% chance to survive five years after their initial diagnosis. This is largely due to relapses, refractory disease, or serious side effects associated with current therapies (i.e. chemotherapy and/or blood stem cell transplantation). To develop better treatment strategies, we must first understand the underlying molecular mechanisms that initiate and maintain the disease.

Loss-of-function mutations in the transcription factor GATA2 occur in 3.4% of AML cases, suggesting that GATA2 is a key regulator of AML. Indeed, we recently identified GATA2 as a tumor suppressor of this disease (Katerndahl, C.D.S. et al. 2021). However, it remains unclear how GATA2WT suppresses AML and how GATA2 mutations interfere with this process. 

Our lab utilizes state-of-the-art techniques to elucidate the mechanisms that GATA2 utilizes to regulate the self-renewal and transformation of myeloid progenitor cells. A greater understanding of these processes may help us to design novel therapeutic strategies to more specifically and effectively treat AML. In addition, identifying the genes and mechanisms that control self-renewal could have important implications for regenerative medicine and stem cell biology.

Identify the transcriptional and epigenetic changes induced by inherited GATA2 mutations

The Katerndahl lab has developed a novel Gata2 mouse model to study how regulates AML. Using cutting-edge technologies such as single cell RNA sequencing, ATAC, ChIP-seq, CUT&RUN, and whole genome bisulfite sequencing, the Katerndahl lab will nominate candidate target genes for functional validation.

Determine the global protein interactions of GATA2

We are using proteomic approaches to identify the global protein interactions of GATA2. Such interactions may be targetable using small molecule inhibitors for therapeutic benefit.

Functionally validate the genes and protein interactions that are regulated by GATA2

Our lab utilizes CRISPR/Cas9 genome editing and Covid-19 mRNA vaccine-based technology to functionally validate the genes and protein interaction that GATA2 regulates. Targets that are identified as functionally relevant in AML pathogenesis will be leveraged for translational studies.

A full list of publications by Casey Katerndahl, PhD, is available on PubMed.

Casey Katerndahl, PhD
Assistant Professor of Pathology and Laboratory Medicine