Latest work by the Glioma Longitudinal Analysis Consortium is out! We integrated genomic, pathology, and microscopy approaches to discover common molecular paths gliomas take following therapy. ➡️ @CellCellPress link: https://t.co/alhOZ1Ll1p A 🧵on what we learned (1/10):

We are thrilled to have published our recent findings regarding the way that GBM tumours adapt to, and survive, treatment in @GenomeBiology. This brief thread highlights what we found: 1/8

It's Ph.D. application season! Ready for the next step in your scientific career? #PhDchat Learn more & apply for JAX's exceptional Ph.D. program in mammalian genetics, neuroscience, or biomedical sciences:

Online Now: Transcriptome analysis reveals tumor microenvironment changes in glioblastoma

I want to thank my postdoctoral advisor, @roelverhaak, my PhD advisor, @chengchao12, the @JCCFund, as well as all my colleagues at JAX and in the brain tumor research community for their support. As a faculty, I plan to pay it forward

Today is officially my first day as an Assistant Professor at @jacksonlab in Farmington, CT. My lab will be applying genomic and pathology approaches to examine how the tumor microenvironment shapes evolution and treatment resistance in diffuse glioma

We think we've found something v.interesting 🧐:IDHwt GBMs can be stratified by treatment response which might inform targeted therapies. Read our study here: https://t.co/VHp0numYEV Funded by @UKRI_News @BRUKresearch @DiMeN_Diversity @LDShospcharity @OscarsCharity @YorkshireBTC

We just published in Neuro-Oncology 🥳 GBMdeconvoluteR quantifies immune & neoplastic cells in bulk RNAseq of IDHwt GBM: https://t.co/i2mGyHXwjd. More research facilitated by @LeedsNeuroRTB funded by @YorkshireBTC and @OscarsCharity.

Congratulations to former summer student @Gordon_Y_Ye!

🎉 Congrats to @jacksonlab Summer Student alumni Emma Wade (left) & Gordon Ye (right) for being selected as 2023-24 Churchill Scholars! This competitive scholarship covers one year of master’s study at @ChurchillCol, a stipend and travel costs. Read more: https://t.co/GhuJ4SZEhT

We'd love to hear back from the community about GBMdeconvoluteR, our tool to infer relative proportions of cancer & TME cells from bulk GBM RNAseq data https://t.co/7J3ndWWpCv Made possible thanks to funding from @UKRI_News @YorkshireBTC @OscarsCharity @3DBioImaging @BNS_updates

Very happy to share our latest manuscript @CellCellPress with you: https://t.co/SpzebU9RIM TL;DR: Glioblastomas are incurable brain tumors colonizing the entire brain. We overlay molecular and functional data to uncover a hijacking of neuronal mechanisms driving invasion.

Spatially resolved multi-omics deciphers bidirectional tumor-host interdependence in glioblastoma

Good morning

The Jane Coffin Childs Memorial Fund (@JCChildsFund) for helping fund this work; and finally, the patients and their families whose donations made this study possible (10/10)

Thanks for reading! It was an honor to work with so many great people on this project. I want to highlight @Kevin_C_Johnson, @JanMartinek1, @PaluckaLab, and the GLASS pathology team for their contributions; my mentor, @roelverhaak, and GLASS leadership for the guidance; (9/10)

To conclude, we integrate these cellular, histological, and genomic changes to group tumors into the three recurrence phenotypes we observe: Neuronal, Mesenchymal, and Proliferative. We believe this grouping offers a framework to help understand why gliomas recur (8/10)

In IDH-mutant tumors we did not observe as many changes in the microenvironment. Instead, these tumors were more proliferative at recurrence, with the largest changes occurring in tumors that acquired hypermutation and deletions of the cell cycle regulator CDKN2A (7/10)

At the same time, a subset of IDH-wild-type tumors took on a mesenchymal phenotype at recurrence. Within these tumors, the myeloid cells and tumor cells expressed several ligand-receptor pairs together suggestive of coordinated signaling interactions (6/10)

Recurrent IDH-wild-type tumors more frequently infiltrated into the normal brain, and their tumor cells up-regulated neuronal signaling programs consistent with “neuron-like” behavior. It's early but this suggests a role for neurons in driving glioma growth post-treatment (5/10)

Our main conclusion: The two major subtypes of diffuse glioma evolve in distinct manners, where IDH-wild-type tumors are driven by microenvironment interactions and IDH-mutant tumors evolve through genetic mechanisms (4/10)