Dana graduated from the University of Vermont in 2017 with a degree in Medical Laboratory Sciences and a minor in Microbiology with departmental honors. She spent three of her undergraduate years researching the role a non-essential mitotic motor protein might have in sensitizing colorectal cancer cells to radiation. After graduating, Dana worked in a hospital laboratory doing clinical microbiology. She joined the PIBS program at the University of Michigan in August of 2020 with hopes of doing translational cancer research and found her niche in the lab of Dr. Carl Koschmann studying pediatric brain cancer. She loves to spend her free time traveling, hiking, and watching Netflix.
Diffuse midline glioma (DMG) is among the most lethal of all childhood cancers. Due to lack of effective therapies and its aggressive phenotype, median survival is less than 18 months, indicating a need to uncover the molecular mechanisms and develop targeted therapies for these patients. Lysine-to-methionine (K27M) substitutions in histone H3 variant H3.3 is present in about 63% of DMG and is often found in conjunction with mutations in the chromatin remodeler ATRX. H3K27M gain-of-function mutations lead to a decrease in repressive epigenetic marks and an increase in activating marks. However, the cell cycle regulator p16 remain repressed with the H3K27M mutation, leading to an increase in cell proliferation. Mutations in ATRX can also lead to epigenetic and cell cycle dysfunction. However, it is not currently well understood why H3K27M and ATRX mutations often occur together or what the implications are on cell cycle and epigenetic regulation. My primary project aims to define the mechanism through which ATRX loss occurs in H3K27M mutant cells, and what the effects are of co-mutation with H3K27M on epigenetic control of cell cycle regulators.
Neurosphere and adherent cell culture, IF and IHC, molecular and cellular techniques