Omer Ali Bayraktar
@bayraktarlab.bsky.social
210 followers 210 following 27 posts
Group leader @sangerinstitute.bsky.social Neural diversity, spatial transcriptomics, glia, GBM
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Reposted by Omer Ali Bayraktar
drjimmylee.bsky.social
📢 @bayraktarlab.bsky.social & colabs at @sangerinstitute.bsky.social are assembling the @opentargets.org funded Neuroimmune Team 🧠🧬-Leverage AI to uncover neurodegeneration

Tech Spec: sanger.wd103.myworkdayjobs.com/en-US/Wellco...
Postdoc AI: sanger.wd103.myworkdayjobs.com/en-US/Wellco...
bayraktarlab.bsky.social
Very excited about our new chapter with @mhaniffa.bsky.social !
mhaniffa.bsky.social
I am excited to begin my new journey as the Head of Cellular Genomics @sangerinstitute.bsky.social

We will decode and recode tissue ecosystems using AI + big data…

Our amazing faculty include Roser Vento-Tormo, @bayraktarlab.bsky.social, Mo Lotfollahi, Sam Behjati and Song Chen..
sangerinstitute.bsky.social
Our newly appointed Head of the Cellular Genomics programme, @mhaniffa.bsky.social, shares her career journey and vision for the future of the programme. Read more below. ⤵️

sangerinstitute.blog/2025/05/20/i...
bayraktarlab.bsky.social
Grateful to >60 authors for their amazing work + @wellcomeleap.bsky.social (special thx to Jason Swedlow for leading DeltaT!) & @cziscience.bsky.social for their support. @ebi.embl.org @crick.ac.uk @cambridgeuni.bsky.social @dkfz.bsky.social @sangerinstitute.bsky.social
bayraktarlab.bsky.social
There are many implications & LOTS of detail in the preprints (e.g. mesenchymal cancer states is really a gliosis/hypoxia response & GB tumour subtypes are likely confounded) bit.ly/4mkrWgs bit.ly/3FbI6Ic
bayraktarlab.bsky.social
Taken together, these 2 studies start to unveil what i call the “rules” of glioblastoma. Despite their incredible complexity, these tumours are governed by specific cellular & tissue mechanisms. We believe/hope this understanding will be a foundation for new therapies
bayraktarlab.bsky.social
In GB, as opposed to unrestrained plasticity of cancer cells, we predict transition highways and barriers aligned with paper 1. And we mechanistically validate a transcriptional repressor safeguarding neuronal like cancer states!
bayraktarlab.bsky.social
scDORI enables us to examine GRNs in a continuous manner across cellular trajectories. Hence, you don’t just map GRNs / TF regulators, you can actually infer cell plasticity and predict the future state of a given cell
bayraktarlab.bsky.social
Here we developed a new deep learning based GRN inference framework: scDORI. See the thread from Manu for more details but few highlights here bsky.app/profile/manu...
manusaraswat.bsky.social
🧠 Excited to share my main PhD project! We mapped the regulatory rules governing Glioblastoma plasticity using single-cell multi-omics and deep learning. This work is part of a two-paper series with @bayraktarlab.bsky.social @oliverstegle.bsky.social and @moritzmall.bsky.social, Preprint at end🧵👇
bayraktarlab.bsky.social
In paper 2, we leverage our massive snRNA-ATACseq data to predict cancer cell state transitions & trajectories from gene regulatory networks. Led in @oliverstegle.bsky.social and Moritz Mall's labs by @manusaraswat.bsky.social @lauraruedag.bsky.social Elisa + Tannia & Fani
bayraktarlab.bsky.social
Hence, we define a stereotyped trajectory of cancer cells at the heart of GB heterogeneity - unifying previously defined cell states & tumour subtypes
bayraktarlab.bsky.social
Finally, cancer cells are not riding alone. We found that this cancer cell trajectory is intimately linked to myeloid heterogeneity and unfolds across regionalised myeloid signalling environments.
bayraktarlab.bsky.social
This led to a wonderful side quest: we mapped tumour subclones in space! We developed SpaceTree to deconvolve tumour subclones in Visium data and found that they are finely spatially intermixed (within Visium spots) in the tissue! github.com/PMBio/spaceT...
bayraktarlab.bsky.social
These results suggest that this trajectory cuts across the genetic hierarchy of GB i.e. shared across tumours/subclones. We used spatial DNA-seq (LCM-WGS) to validate this +found the trajectory is shared, yet genetically malleable.
bayraktarlab.bsky.social
Unbiased transcriptomic trajectory analysis (i.e. our cell2fate RNA velocity go.nature.com/4km62aI) finds that this is trajectory shared across tumours + genetic subclones. And we define a molecular progression conserved across tumours/clones
bayraktarlab.bsky.social
When you look into the tumour areas/states dominated by gliosis/hypoxia, these transitions become clear. You can see cancer cells travelling from developmental astrocyte like states gradually into gliosis + hypoxia response (more on this below)
bayraktarlab.bsky.social
..to resolving this trajectory. Integrating single nuclei + spatial data revealed stepwise spatial transitions of cancer cell states from the tumour invasive edge towards the necrotic core. This looked like spatially organised cancer cell transitions as GB tumours rapidly expand.
bayraktarlab.bsky.social
It started with single nuclei RNA-seq. Profiling >1 million cells, we saw within each tumour that cancer cells vary from developmental progenitor-like states (e.g.NPC/OPC) to those marked by gliosis (i.e. glial injury response) & hypoxia Yet, the spatial/tissue context was the key…