Dana Messinger

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 cancer research and found her niche in the lab of Dr. Carl Koschmann studying high-grade pediatric brain tumors. She loves to spend her free time traveling, hiking, and attending concerts.

Pediatric high-grade glioma (pHGG), which includes diffuse midline glioma (DMG), are among the most lethal of all pediatric cancers, with survival rarely exceeding 2 years. The most common mutations in pHGG are found in histone variant H3.3 (H3F3A), with nearly 50% of all pHGG exhibiting gain-of-function mutations at either lysine 27 (K27M) or glycine 34 (G34R/V). Both histone mutants result in widespread epigenetic impacts on transcriptional control and distinct clinical behavior1. Additionally, roughly 30% of pHGG harbor loss-of-function mutations in the chromatin remodeling protein ATRX, which co-occur in about 20% of H3K27M tumors and 90% of those with H3G34R/V mutations. Little is known as to why ATRX mutation co-occurs almost five times as frequently with G34R/V mutation, and no studies have addressed whether ATRX plays a different role in tumor development depending on the concurrent H3.3 mutation. The activity of EZH2, the catalytic subunit of the polycomb repressive complex 2 (PRC2), is known to be impaired by H3K27M, but it is also thought that ATRX plays a role in proper EZH2 function. PRC2 is critical for maintaining repression of many early developmental genes, including those involved in early brain development. The objective of my project is to determine how ATRX loss impacts developmental gene expression in H3G34R/V mutant tumor cells compared to H3K27M mutant cells.

Neurosphere and adherent cell culture, IF and IHC, molecular and cellular techniques

Therapeutic targeting of prenatal pontine ID1 signaling in diffuse midline glioma 

a. Top Biospecimens Award, Children's Brain Tumor Network (CBTN) Scientific Summit Poster session, 17 October 2022, Washington, D.C.

Therapeutic targeting of prenatal pontine ID1 signaling in diffuse midline glioma

a. 5-minute oral rapid report presentation, Society for Neuro-Oncology (SNO) Annual Scientific Meeting, 18 November 2022, Tampa, FL.

https://www.ncbi.nlm.nih.gov/myncbi/dana.messinger.1/bibliography/public/