New paper alert! In this study, we find that cells with chromosomal instability (CIN) secrete more extracellular vesicles (EVs). These CIN-induced EVs promote migration and invasion of EV-recipient cells an EFEMP1-dependent manner both in vitro and in vivo. link.springer.com/article/10.1...

Chromosomal instability promotes cell migration and invasion via EFEMP1 secretion into extracellular vesicles - The EMBO Journal

Triple-negative breast cancer (TNBC) is characterised by high rates of chromosomal instability (CIN) and rewired intercellular communication driven by both soluble factors and extracellular vesicles (...

link.springer.com

Mitotic BLM functions are required to maintain genomic stability url: academic.oup.com/nar/article/...

Mitotic BLM functions are required to maintain genomic stability

Abstract. The BLM helicase is a critical genome maintenance protein involved in diverse cellular processes including DNA replication, repair, transcription

academic.oup.com

Breast cancer cells with chromosomal instability (CIN) promote cell migration and invasion of low-CIN cancer cells via secretion of extracellular vesicles transferring ECM components @foijer-lab.bsky.social and collaborators link.springer.com/article/10.1...

Chromosomal instability promotes cell migration and invasion via EFEMP1 secretion into extracellular vesicles - The EMBO Journal

Triple-negative breast cancer (TNBC) is characterised by high rates of chromosomal instability (CIN) and rewired intercellular communication driven by both soluble factors and extracellular vesicles (...

link.springer.com

Very proud that so many of our team will be joining a Dutch winter biathlon (10K skating + 90K cycling) through Dutch winds to raise money for lymphoma research. Read more here: www.dehollandse100.nl/teams/cinners

Mitotic BLM functions are required to maintain genomic stability url: academic.oup.com/nar/article/...

Mitotic BLM functions are required to maintain genomic stability

Abstract. The BLM helicase is a critical genome maintenance protein involved in diverse cellular processes including DNA replication, repair, transcription

academic.oup.com

👋 To all aneuploidy and chromosome instability aficionados check out the Consequences of Aneuploidy FASEB conference (Florida-USA 🏖️) co-organised with @peterlylab.bsky.social, Mike Lampson, Alison Taylor and myself: events.faseb.org/event/Aneupl... 👉 Deadline for abstract submission: August 3rd.

A role For BLM in mitosis preserving genomic integrity. Very interesting read with very elegant experimental approaching including some some must have single cell genomics. ;) academic.oup.com/nar/article/...

Very beautiful work to which we made a small contribution. Congrats to @eileenparkes.bsky.social and team! #CIN #Immunesurveillance| Science Advances www.science.org/doi/10.1126/...

Chromosomal instability shapes the tumor microenvironment of esophageal adenocarcinoma via a cGAS–chemokine–myeloid axis

Chromosomal chaos rewires immune defense into tumor-promoting inflammation.

science.org

#1 Centromeres are epigenetic loci defined by CENP-A, positioned in unmethylated DNA flanked by highly methylated regions. Our work, published in @natgenet.nature.com in collaboration with @naltemose.bsky.social investigates the role of DNAme at human centromeres www.nature.com/articles/s41...

DNA methylation influences human centromere positioning and function - Nature Genetics

Genome-wide and targeted perturbation of DNA methylation at centromeres affects CENP-A positioning and centromere structure, resulting in aneuploidy and reduced cell viability.

nature.com

📢ONLINE @natgenet.nature.com 📰DNA methylation influences human centromere positioning and function. By Catalina Salinas-Luypaert, @dfachinetti.bsky.social, @naltemose.bsky.social and colleagues. ⬇️ www.nature.com/articles/s41...

DNA methylation influences human centromere positioning and function - Nature Genetics

Genome-wide and targeted perturbation of DNA methylation at centromeres affects CENP-A positioning and centromere structure, resulting in aneuploidy and reduced cell viability.

nature.com

Using barcodes 📊 to track cancer 💊 resistance evolution: is it clonal selection or plasticity? @fwhiting.bsky.social‬ knows! His new "Evolutionary Informed Resistance Assays" (EIRAs) framework infers resistance evolution dynamics from barcode diversity data. www.nature.com/articles/s41... @icr.ac.uk

Quantitative measurement of phenotype dynamics during cancer drug resistance evolution using genetic barcoding - Nature Communications

Understanding the dynamics of how drug resistance originates in cancer remains crucial, but it is not possible to observe them directly. Here, the authors construct a mathematical framework to infer d...

nature.com

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)

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...

science.org

🧬 New tool to generate aneuploidies and analyse their impact on development. The tool created by @milanlab.bsky.social helps better understand this phenomenon, which is the main cause of spontaneous miscarriage. 📰 Published in #CellGenomics by #IRBBarcelona Read the news ➡️ shorturl.at/Ektif 👇

👋 Are you looking for a postdoc position? Do you think microtubules are fascinating? Then we might have the job for you! 2-year funded postdoc to join our lab! 👉 deadline 20/06 👇 check it out www.godinholab.com

No brainer for talented bioinformaticians: great team, great science, great mentor! Apply!

@dfachinetti.bsky.social · last yr.

Hi all, my team institut-curie.org/team/fachine... @institutcurie.bsky.social is looking for a Bioinformatician. You can find more details about the position here: euraxess.ec.europa.eu/jobs/344508 Is anyone looking for a job in the lovely Paris?

Incoming - new preprint alert from the Parkes lab led by @brunobeernaert.bsky.social Full bluetutorial follows! 1/ 11 www.biorxiv.org/content/10.1...

The @embo.org #chromoploidy2025 is over. It was an amazing workshop organized by a perfect match of scientists and friends @mcclellandlab.bsky.social @bendavidlab.bsky.social @stesantaguida.bsky.social @foijer-lab.bsky.social, Elsa Logarinho, Caroline Audouin and myself

Excited to get the #EMBOChromoploidy meeting started! 3 days of fantastic science and fun in beautiful Stresa are beginning now! meetings.embo.org/event/25-ane...

Chromosome Segregation and Aneuploidy

Aneuploidy is a hallmark of cancer and developmental disorders such as Down syndrome. Understanding how cells accomplish faithful chromosome segregation and how chromosomal instability (CIN) impacts …

meetings.embo.org

Super cool new preprint: FANCD2:FANCI is a sensor of open chromatin, independent of DNA damage, but further increased at double strand breaks. www.biorxiv.org/content/10.1...

The FANCD2-FANCI heterodimer coordinates chromatin openness and cell cycle progression throughout DNA double-strand break repair

The FANCD2-FANCI heterodimer contributes to DNA repair at interstrand crosslinks and sites of replication stress. This complex has been physically and mechanistically linked to double-strand break (DSB) repair, but its role in that process remains undefined. Here we show that the FANCD2-FANCI heterodimer dynamically interacts with open chromatin regions, including transient, DSB-induced open chromatin, where it can be stabilized by co-activation by the DNA repair kinase ATM and the Fanconi anemia core ubiquitin ligase. The loaded FANCD2-FANCI heterodimer stabilizes open chromatin and promotes resection and loading of RPA through increased association of BRCA1 and BLM. Chromatin-loaded FANCD2-FANCI has a second distinct function promoting a G2 arrest that is dependent on the ATR-CHK1-WEE1 axis. Our results support a two-step genome surveillance model in which FANCD2-FANCI monitors open chromatin sites and is stably loaded to coordinate DNA repair activities in response to signaling from a DNA repair kinase. ### Competing Interest Statement The authors have declared no competing interest.

biorxiv.org

Delighted to share a chemical-genetic system we developed to rapidly inhibit a serine/threonine phosphatase complex (within secs). This will make it much easier to study #phosphatases. The system is also applicable to other “undruggable” enzymes. www.nature.com/articles/s41...

A chemical-genetic system to rapidly inhibit the PP2A-B56 phosphatase reveals a role at metaphase kinetochores - Nature Communications

Phosphatase enzymes are challenging to study due to a lack of specific inhibitors. Here, authors develop a chemical-genetic system to inhibit and characterize a major Ser/Thr phosphatase complex, and ...

nature.com

We now have a Twitter account, to reach people who are not on bluesky—and to help get them here. If you still have a Twitter account please follow us there, and ask others to follow too. x.com/altnih4science

A window-of-opportunity trial reveals mechanisms of response and resistance to navtemadlin in patients with recurrent glioblastoma | Science Translational Medicine www.science.org/doi/abs/10.1...

A window-of-opportunity trial reveals mechanisms of response and resistance to navtemadlin in patients with recurrent glioblastoma

In patients with glioblastoma, navtemadlin resistance is not mediated by TP53-inactivating mutations, and combination with TMZ may improve efficacy.

science.org

Please check out our preprint where we find that mitotic transcription helps ensure ecDNA inheritance through chromosomal tethering: www.biorxiv.org/content/10.1...

Dear all, Postdoc positions are available to work on (1) the role of DNA strand break repair proteins during DNA replication and (2) the molecular/structural biology of XRCC1 protein complexes, as part of our work on genetic diseases & cancer. Contact me if interested: k.w.caldecott@sussex.ac.uk

Supper happy to see the results of our longstanding collaboration in @naturecomms.bsky.social. We identify RBM14 as an ARGOS gene to modulate cGAS-STING signalling. Driven by @ms01.bsky.social and @vrendo.bsky.social with @bendavidlab.bsky.social and @rameenberoukhim.bsky.social. rdcu.be/d7Mky

A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer

Nature Communications - In cancer, the impact on cellular fitness of copy-number gains affecting collaterally-amplified genes remains poorly understood compared to oncogenes. Here, the authors...

rdcu.be

New paper out! 🚨🥳 We thought that passenger gene amplifications can drive cancer vulnerabilities and show that RBM14 does so via cGAS-STING modulation 👇 @vrendo.bsky.social @bendavidlab.bsky.social @rameenberoukhim.bsky.social @foijer-lab.bsky.social

Veronica Rendo@vrendo.bsky.social · 2y ago

So excited to see our paper describing the class of ARGOS genes in cancer out in @naturecomms.bsky.social! 🤩 www.nature.com/articles/s41... A giant effort led with @ms01.bsky.social and executed under the mentorship of @bendavidlab.bsky.social @rameenberoukhim.bsky.social @foijer-lab.bsky.social 🧵👇:

So excited to see our paper describing the class of ARGOS genes in cancer out in @naturecomms.bsky.social! 🤩 www.nature.com/articles/s41... A giant effort led with @ms01.bsky.social and executed under the mentorship of @bendavidlab.bsky.social @rameenberoukhim.bsky.social @foijer-lab.bsky.social 🧵👇:

A compendium of Amplification-Related Gain Of Sensitivity genes in human cancer - Nature Communications

In cancer, the impact on cellular fitness of copy-number gains affecting collaterally-amplified genes remains poorly understood compared to oncogenes. Here, the authors integrate genomic data from tum...

nature.com

High CDC20 levels increase sensitivity of #cancer cells to MPS1 inhibitors. -> www.embopress.org/doi/full/10.... High CDC20 expression promotes aneuploid cancer #cell sensitivity to #spindle assembly #checkpoint (SAC) inhibition by prolonging #metaphase and reducing mitotic errors.

@bendavidlab.bsky.social · 2y ago

Happy to share our new paper, published in @emboreports.org, in which we identify CDC20 as an important determinant of the cellular response to SAC inhibition. close collaboration with the @foijer-lab.bsky.social. Kudos to Linoy, Siqi and Lin for spearheading this study! 👏 Link in 1st comment 😊

CDC20 is a modulator of CIN, too much CDC20 promotes CIN, too little CDC20 decreases sensitivity to spindle checkpoint inhibitors. A very fruitful collaboration between the @bendavidlab.bsky.social and our lab. Check out our publication here: www.embopress.org/doi/full/10....

The Foijer lab is making a new start @bsky.app, moving away from X. We will continue to update you of our science news and share news of others as previously, and maybe even a bit more proactively :). Let's stay in touch!