Sarah Moser

The latest work from ours and @vram142.bsky.social lab is out! True teamwork to visualize nascent chromatin with strand resolution, using a fully reconstituted system. Very proud of superstar-PhD student Bruna, and @palindromephd.bsky.social. Learning so much from Vijay’s amazing technologies! RT

Check out the full story here: rdcu.be/eGm9f

Histone Recycling Promotes PARP Inhibitor Resistance Major Finding: PARP inhibition induces eviction of histones, and the chaperone NASP is required to recycle these histones to prevent DNA damage and promote resistance. Concept: Histone recycling repre...

Thank you @aacrjournals.bsky.social for highlighting our recent study on PARP inhibitors and histone turnover! 🧬💊

Big congratulations to @sarahmoser.bsky.social @oncodeinstitute.bsky.social for being named a 2025 International Birnstiel Award laureate!

Selected from 87 nominations, Sarah is one of just six doctoral researchers worldwide to receive this prestigious recognition in molecular life sciences.

Honoured (and excited!) I was named among this year's Birnstiel awardees for my PhD work! 🎉

Breaking the chain: uncovering a hidden weakness in PARP-resistant cancers ➡️ www.nki.nl/news-events/...

#fundamentalresearch #cancerresearch #NKI #breastcancer #ovariancancer

NASP modulates histone turnover to drive PARP inhibitor resistance - Nature PARP inhibitor treatment triggers histone release from the chromatin in cancer cells; consequently, targeting the histone chaperone NASP renders cells vulnerable to PARP inhibition.

Nature research paper: NASP modulates histone turnover to drive PARP inhibitor resistance

go.nature.com/45vRWhd

Thank you so much for your help and probably the fastest collaboration in history!

The nuclear periphery confers repression on H3K9me2-marked genes and transposons to shape cell fate - Nature Cell Biology Marin et al. report the role of lamin proteins and the lamin B receptor (LBR) in chromatin positioning at the nuclear periphery. Knockout of all lamins and LBR in mouse embryonic stem cells leads to h...

Another paper bluetorial! Today: how does the spatial location of genes influence their function? (1/n) www.nature.com/articles/s41...

@akhalizieva.bsky.social @milokaptein.bsky.social @icrlordlab.bsky.social @fmattiroli.bsky.social @thijnbrummel.bsky.social and all our blueskyless collaborators

I am also extremely thankful to my fellow lab members at @nkinl.bsky.social and our internal and external collaborators, whose expertise and dedication brought this project over the finish line. (8/8)

This project has been a truly exciting chapter of my PhD journey and I am deeply grateful to everyone involved. A heartfelt thank you to my mentors, @josjonkers.bsky.social and @amazouzi.bsky.social for their guidance in solving the histone puzzle.

💡 Take-home: Histone eviction is an immediate response to PARPi treatment and cancer cells are require an INO80–NASP–PARP1 axis for survival. Targeting histone turnover could therefore overcome drug resistance. (7/8)

However, NASP cannot do it all. It is supported by (1) the INO80 complex which remodels chromatin to evict histones, (2) which NASP then stabilises and stores and (3) PARP1 and other factors help reincorporate them. (6/8)

Lose NASP and even resistant tumor cells become resistant to PARPi. (5/8)

What are the factors mediating this histone release? To answer this we performed genome-wide genetic screens and identified NASP, a histone chaperone, as essential for handling these evicted histones. (4/8)

The answer was puzzling: Histones got kicked off the chromatin upon PARPi exposure. These free histones must be stored & recycled, otherwise cancer cells struggle to survive. (3/8)

PARP inhibitors (PARPi) have clearly been a game changer for homologous recombination-deficient tumours, but therapy resistance remains a challenge. The impact of PARPi on DNA integrity has been very well described, but we wondered what happens to the chromatin environment? 🧬 (2/8)

NASP modulates histone turnover to drive PARP inhibitor resistance - Nature PARP inhibitor treatment triggers histone release from the chromatin in cancer cells; consequently, targeting the histone chaperone NASP renders cells vulnerable to PARP inhibition.

Thrilled to share our latest work, just published in @nature.com ⬇
www.nature.com/articles/s41...

We discovered that PARP inhibitors 💊 trigger histone eviction from the chromatin and this creates a hidden vulnerability in PARPi resistant tumors.
🧵 (1/8)

🗓️ @mylliabio.bsky.social sponsors the first conference on "High-Content CRISPR Screening" from March 18-19, 2026 in Vienna: perturb2026.bio

Scientific topics:
🔬 CRISPR-based screening strategies
🧬 Perturb-Seq & CROP-Seq
💻 Computational analyses
💻 AI models of human cells
📸 Image-based screens

New online! Making sense of the polygenicity of complex traits

RNA transcripts regulate G-quadruplex landscapes through G-loop formation G-quadruplexes (G4s) are prevalent DNA structures that regulate transcription but also threaten genome stability. How G4 dynamics are controlled remains poorly understood. Here, we report that RNA tra...

Excited our paper is out! G-quadruplex (G4) unwinding via an intricate G-loop assembly and disassembly mechanism maintains genome integrity. Pioneered by Koichi Sato with great collaborators Jing Lyu and @simonelsasser.bsky.social Check it out: www.science.org/doi/10.1126/science.adr0493 🧵(1/4)

Acquired resistance in cancer: towards targeted therapeutic strategies - Nature Reviews Cancer Acquired therapeutic resistance is a key contributor to cancer treatment failure, requiring new approaches to address its complex mechanisms. In this Roadmap, Soragni, Knudsen and colleagues discuss the mechanisms of acquired resistance and the models to better study it. Finally, they promote integration of biomarker-driven strategies and cutting-edge technologies to advance predictive and proactive prevention in cancer therapy.

🚨Roadmap 🚨
Alice Soragni @alice.soragnilab.com‬, Erik S. Knudsen ‪@roswellpark.bsky.social‬ ‪ & Co discuss the mechanisms of acquired resistance and the models to better study it to advance predictive and proactive prevention in cancer therapy.
📖 ⬇️

Today, these amazing NKI researchers are pushing their limits by climbing the Alpe d’Huez. Go for it lovely people! We are proud to see so many of you dedicate your time and effort to supporting cancer research.
With @oncodeinstitute.bsky.social

#AlpedHuZes #cancerresearch #ad6 #NKI

Excited to share our preprint on the molecular architecture of heterochromatin in human cells 🧬🔬w/ @jpkreysing.bsky.social, @johannesbetz.bsky.social,
@marinalusic.bsky.social, Turoňová lab, @hummerlab.bsky.social @becklab.bsky.social @mpibp.bsky.social

🔗 Preprint here tinyurl.com/3a74uanv

We’re excited to share our work where we investigated the mechanisms of chromosome motion by tracking all #chromosomes, mapping their interactions, and live cell karyotyping, using #AI based denoising, segmentation and registration, published in Nature Cell Biology.
www.nature.com/articles/s41...

title, authors and abstract Sequence-dependent activity and compartmentalization of foreign DNA in a eukaryotic nucleus https://pubmed.ncbi.nlm.nih.gov/39913590/

In a remarkable new paper researchers take a very unconventional approach, introducing into yeast cells (S. cerevisiae) entirely new chromosomes whose DNA never existed in a eukaryotic nucleus. They do this by making the entire bacterial genome of two different bacteria into a yeast chromosome 3/n

Paired-Damage-seq is an in situ labeling-by-repair strategy for joint profiling of oxidative and ssDNA damage alongside gene expression, in single cells.

www.nature.com/articles/s41...

Our new findings on how chromosomes get ready for cell division are now published in @cellpress.bsky.social!

Congratulations, Kai, @andibrunner.bsky.social and everyone else involved! 🤩

www.sciencedirect.com/science/arti...

📢The programme for #DDRCT25 is now available! Visit our website to explore the exciting sessions, speakers, and key topics we have in store.
➡️Check it out here: fusion-conferences.com/conference/177