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.
Pediatric high-grade gliomas (pHGGs), including diffuse intrinsic pontine glioma (DIPG), are the most lethal of all childhood cancers, with a median survival between 12 and 18 months. This indicates an urgent need to elucidate the molecular mechanisms and develop appropriate targeted therapies for these patients. Lysine-to-methionine (K27M) substitutions in histone H3 variant H3.3 is present in about 63% of DIPG and is often found in conjunction with mutations in ATRX. H3K27M gain-of-function mutations lead to a decrease in the repressive trimethylation mark and an increase in the activating acetylation at K27 at many gene loci, leading to dysregulation of various cell cycle and DNA damage repair (DDR) genes. Mutations in ATRX, a chromatin remodeling protein, can also lead to dysregulation of cell cycle regulatory genes and DDR. However, it is not currently well understood why H3K27M and ATRX mutations often occur together or what the implications are on cell cycle control and DDR. We expect to define the mechanism through which ATRX loss results in cell cycle dysregulation, and what the effects are of co-mutation with H3K27M on epigenetic control of cell cycle regulators and DDR.
Neurosphere and adherent cell culture, Immunohistochemistry, Immunofluorescence