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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
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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