Weekly reads: our new brain tumor paper, levitation, dear doctor, Japan, more

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There’s nothing quite like getting a new paper out as a scientist running a research lab so this week we can celebrate our new pediatric brain tumor study. I’ll start the weekly reads with that paper. Of course, getting new grants is amazing too but there’s more of a feel of completion after a paper gets published. Grants are more about the future.

Brain tumor functional network K27M
H3.3 K27M brain tumor functional network mapping identifies predicted interconnected ASCL1 and NEUROD1 nodes. Lewis, et al. Epigenetics & Chromatin 2022.

Brain tumor research

Histone H3.3 K27M chromatin functions implicate a network of neurodevelopmental factors including ASCL1 and NEUROD1 in DIPG, Epigenetics & Chromatin. My student, now Dr. Nichole Lewis, Ph.D., did great work on this new study, which was a team effort. Through using ATAC-Seq, she was able to define regions of chromatin accessibility related to the histone H3.3 K27M mutation. We also integrated this data with our past RNA-Seq data on the same cells to identify open regions that in addition had active genes. Nichole used a new method called HINT-ATAC too that enables footprinting of the open regions to define a bit less open domains corresponding to predicted bound transcription motifs. All of this combined together and via network analysis pointed to neurodevelopmental pathways and in particular predicted the bHLH transcription factors ASCL1 and NEUROD1 as being central downstream of K27M. For those of you not intensively into this kind of research, in a nutshell, our study suggests that the machinery that impacts normal neural stem cell and precursor fate gets altered and coopted during childhood glioma by a specific histone mutation leading to too much growth and resistance to differentiation.

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