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Cosmin Tudose

@cosmintudose.bsky.social
61 followers 109 following 17 posts

Postdoctoral researcher @IBCII Perturbation Genomics Lab Omics | Bioinformatics | Cancer

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Reposted by Cosmin Tudose
Noura Maziak @nmaziak.bsky.social · 10/03/2026
Excited to share my PhD work! The question: How is genome organization established? Here, we developed a low-input Micro-C method, Pico-C, and used it to map chromatin architecture across early stages of fly development. Here’s a quick Blue-torial 🙂 (1/n) www.nature.com/articles/s41...
nature.com
Three-dimensional genome reorganization foreshadows zygotic genome activation in Drosophila - Nature Genetics
Pico-C, a low-input Micro-C approach, reveals that dynamic three-dimensional genome folding precedes zygotic genome activation in Drosophila.
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Reposted by Cosmin Tudose
Colm Ryan @colmr.bsky.social · 29/01/2026
New paper from Narod Kebabci – “A predicted cancer dependency map for paralog pairs” www.biorxiv.org/content/10.6... Background: The Cancer Dependency Map from @depmap.org is a fantastic resource that characterises genetic dependencies at genome-wide scale across ~1,000 cancer cell lines. 1/9
biorxiv.org
A predicted cancer dependency map for paralog pairs
Background Genome-wide CRISPR screening has enabled the development of dependency maps in hundreds of cancer cell lines, facilitating the identification of genetic vulnerabilities associated with specific biomarkers. Paralogs, despite being common drug targets, are often missed in these screens as their individual disruption rarely causes a significant fitness defect. Combinatorial screens have revealed that paralog pairs are often synthetic lethal but that these effects are highly context specific. To develop paralogs as therapeutic targets we must identify which paralog pairs are synthetic lethal in which cancer contexts. Results We develop a machine learning classifier to predict cell-line specific synthetic lethality between paralog pairs. We demonstrate the utility of features derived from the cell-line specific expression and essentiality of the pair and their protein-protein interaction partners for this purpose. We evaluate our predictions across multiple scenarios: predicting for the same pairs in unseen cell lines, for new gene pairs in seen cell lines, and for entirely uncharacterized pairs in unseen cell lines. We show that we can make predictions across all scenarios. We validate our predictions using independent combinatorial CRISPR screens and show that the agreement between our predictions and published experiments approaches the agreement across experiments. Conclusions Our classifier predicts cell-line-specific synthetic lethality between paralog pairs and provides insights into the underlying features driving these interactions. We make our predictions for 1,005 cell lines available as a resource to facilitate the discovery of context-specific paralog synthetic lethalities and to guide the design of more targeted combinatorial screens. ### Competing Interest Statement The authors have declared no competing interest. Research Ireland, 20/FFP-P/8641, 18/CRT/6214
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Reposted by Cosmin Tudose
Colm Ryan @colmr.bsky.social · 05/12/2025
Great to see this out, collaboration with the Bond lab @sysbioire.bsky.social to understand consequences of EZH2 mutation in T-acute lymphoblastic leukaemia (T-ALL). Congrats to @lefeivret.bsky.social @cosmintudose.bsky.social and other authors not on bluesky! ashpublications.org/bloodadvance...
ashpublications.org
Reduced PRC2 function causes asparaginase resistance in T-ALL by decreasing WNT pathway activity
Key Points. Reduced PRC2 function in T-ALL is associated with asparaginase resistance that is linked to reduced WNT/STOP pathway activity.Asparaginase resi
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Finally, thanks to @researchireland.ie, CRT Genomics Data science for funding this work! And thanks to @ucddublin.bsky.social @sysbioire.bsky.social for the support offered! 17/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Thanks to my supervisors for guiding this work Jonathan Bond and @colmr.bsky.social and to everyone involved for all the important and hard work put in Luke Jones, Claire Fitzgerald, @tgrosu.bsky.social, @nmaziak.bsky.social Rebecca Ling, @roylab-oxford.bsky.social, @vaquerizasjm.bsky.social 16/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
...leading to partial activation of an onco-fetal LIN28B-driven program that makes AML cells more resistant to CDK6 inhibition. 15/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Our work highlights the role of polycomb in guiding the expression of lineage-defining transcriptional programs and heterozygous loss of EZH2 is enough to blur the lines between transcriptional programs…🌫️14/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Finally, we found that the EZH2-LIN28B-CDK6 axis leads to increased resistance to the CDK4/6 inhibitor palbociclib. 13/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
LIN28B is rarely expressed in normal adult cells, but is active in >20 cancer types, including leukemias. As part of this program we find the cyclin-dependent kinase CDK6, which shows decreased promoter H3K27me3, accompanied by increased H3K27ac and increased transcription. 12/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Finally, we found that our EZH2+/- cells show activation of an alternative lineage transcriptomic program associated with LIN28B activation. Using RNA-seq from LIN28B-KD CD34+ fetal liver cells, we confirmed that EZH2-depleted cells are consistent with LIN28B activation. 11/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Notably, we observed a compartmentalization change upstream of the LIN28B locus in the Hi-C data. While this locus did not show any significant change in H3K27me or H3K27ac, the LIN28B fetal oncogene was upregulated in our EZH2+/- cells. 10/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Secondly, as observed in the Hi-C, these peaks are found in regions where there is high DNA-DNA contact frequency in all conditions, suggesting H3K27me3 is preferentially maintained at these hubs of compacted chromatin ➰➰➰. 9/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Naturally, we observed that some level of H3K27me3 is maintained in EZH2+/- and we found out that these maintained me3 peaks show distinctive characteristics. Firstly, these peaks are wider, covering a larger genomic area🧬. 8/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
However, the relationship between chromatin accessibility and transcriptional activation is complex. As previously shown by Kiani et al. (doi.org/10.15252/msb...), increased chromatin accessibility does not always lead to transcription. 7/17
doi.org
Changes in chromatin accessibility are not concordant with transcriptional changes for single‐factor perturbations | Molecular Systems Biology
image image Systematic analysis of tandem, bulk ATAC‐seq and RNA‐seq measurements from cells exposed to single‐factor perturbations shows two groups of genes: those with concordance between accessibility and expression changes and those ...
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Again, we observed that regions with increased accessibility were enriched for GO terms relating to cell differentiation and alternative transcriptional lineages. 6/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
As expected, we observed genome-wide decrease in the PRC2-mark H3K27me3, accompanied by increased H3K27ac and increased chromatin accessibility. NOTE: C5 and C9 are EZH2+/- cells in the figure below. 5/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
This suggests that PRC2 depletion leads to transcriptional changes related to cell differentiation. But what about direct epigenetic changes?🤔 4/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Strikingly, we observed that at the transcriptomic level the PRC2-depleted showed increased expression of genes typically expressed monocytic-dendritic progenitors (e.g., CDCA7, CDK6), and decreased expression of genes expressed in mature monocytes (e.g., ITGAM, S100A12)🩸. 3/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
We generated a PRC2-depleted model by heterozygously targeting the catalytic component EZH2✍️in OCI-AML2 cells🧫. We then extensively characterized these cells by RNA-Seq, ATAC-Seq, CUT&RUN and Hi-C. 2/17
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Cosmin Tudose @cosmintudose.bsky.social · 09/09/2025
Pleased that the 2nd part of my PhD is now available as a preprint! Here, we investigated the epigenomic and transcriptomic changes occurring upon PRC2 depletion in AML cells. biorxiv.org/content/10.1.... A thread🧵1/17
biorxiv.org
Diverse epigenomic mechanisms underpin transcriptional dysregulation in Polycomb-altered acute myeloid leukemia
Background Polycomb Repressive Complex 2 (PRC2) modulates chromatin accessibility and architecture to direct tissue-specific gene expression. PRC2 function is frequently altered in cancer by loss-of-f...
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