Great conference, great science and great location!

Excited to announce: the EMBO Workshop: DNA damage response in cell physiology & diseases - 12–16 Oct 2026 - in stunning Sounio, Greece - fabulous speaker speaker lineup representing the cutting-edge of genome stability research: Abstract deadline: 17 May meetings.embo.org/event/26-dna... Join us!

Big Congrats Kelly 😊

Data Scientist in Sutton | The Institute of Cancer Research View details and apply for this Data Scientist vacancy in Sutton. Salary : Salary range £39,805 - £53,500 (Salary appointment dependent on experience ) Reporting to: P...

Are you fascinated by cancer biology and also ❤️ 💻 ? Feel like this ->😻<- at the thought of exploring oodles of cancer genomes, single cells and spatial multiomics data? Then our core Data Science Team at @icr.ac.uk might be the place for you. Vacancy here: jobs.icr.ac.uk/vacancies/14...

SET1/MLL complexes control transcription independently of H3K4me3 Histone H3 lysine 4 trimethylation (H3K4me3) at gene promoters is thought to play a central role in gene transcription. H3K4 methylation is deposited by the SET1 (A/B) and MLL (1-4) multi-protein comp...

An early Christmas present for those interested in chromatin and transcription! Fantastic work from @au-ho-yu.bsky.social and @aleksszczurek.bsky.social . Thanks to Inge and Michiel for their help. Please repost!

www.biorxiv.org/content/10.6...

My PhD work is out as a preprint! Have a read 😊👇🏻

Thanks Chris

Special credits go to lead author (& recent lab PhD graduate) @pia-rei.bsky.social and to fantastic collaborators Adam Wilkinson, Ben Davies and Francisca Lottersberger. @ukri.org, CRUK & @thelisterinstitute.bsky.social for funding! Reach out if you have any questions.

Biochemically validated AF3 model of the ERCC6L2-MRI-KU complex

Its DNA structural-specificity is defined using IG class-switching & dysfunctional telomeres with staggered vs blunt DNA ends. Surprisingly, bone marrow HSPCs in ERCC6L2-knockout mice are surprisingly resilient. We therefore speculate as to why bone marrow fails in ERCC6L2-deficient man but not mice

The ERCC6L2-MRI-KU complex coordinates NHEJ at staggered DNA double-strand breaks ERCC6L2 disease is a recessive bone marrow failure (BMF) syndrome caused by mutations in the SNF2-like putative DNA helicase ERCC6L2. While implicated in DNA replication, double strand break (DSB) rep...

New lab preprint! ERCC6L2 disease is a recessive bone marrow failure syndrome caused by mutations in the putative DNA helicase ERCC6L2. Using mouse genetics, biochemistry and AF3 we uncover ERCC6L2-MRI as a KU-regulatory complex stimulating NHEJ at staggered DSBs: www.biorxiv.org/content/10.1...

When the work of your colleagues really blows your mind 🤯🔥. Congratulations @jojdavies.bsky.social, team and collaborators! 🥂

Actual Social DNAing Webinar Social DNAing Weekly Webinar Serial hosted by Columbia University College for Physicians and Surgerons. The channel host the webinar from preivious week with permission from the speaker.

Thanks Shan Zha for hosting my Social DNA’ing on Thursday. Was a honour to celebrate the 5th anniversary of this epic series. If you didn’t catch it, pls check out the recorded webinar to find out what we’ve been up to with research support from @cruk-ci.bsky.social! fast.wistia.com/embed/channe...

Congrats Kelly! 🥂

Excited to share our new paper on Nature - how Ku accommodates Alu expansion in primates by binding to dsRNA, providing a clue for both the high levels of Ku and its essentiality in human cells. Thank @chaolinzhang @hchung03 @LenaSteckelberg More to come www.nature.com/articles/s41...

Breast cancer gene families given hope by drug trial Treating patients with a drug before surgery greatly reduced the chances of the cancer coming back, a small trial found.

A new treatment significantly improves survival rates for women with aggressive, inherited breast cancer involving BRCA1 or BRCA2 gene mutations.

Giving them the targeted drug olaparib before surgery greatly reduced the chances of the cancer coming back.

🧪🧬💊 #medsky
www.bbc.com/news/article...

César Milstein Lecture David Pellman Dana-Farber Cancer Institute, Harvard University Mechanisms driving the rapid evolution of genomes Thursday 24 April at 10 am Max Perutz Lecture Theatre and Zoom Details on the LMB website Sponsored by AstraZeneca

Don’t miss the 2025 César Milstein Lecture, by David Pellman from the Dana-Farber Cancer Institute and Harvard University.
Join us at 10am (BST) on Thu 24th April to learn about “Mechanisms driving the rapid evolution of genomes”
More details: www2.mrc-lmb.cam.ac.uk/news-and-eve...
#LMBSeminar

Please repost! Post-doc studying novel mechanisms of post-replicative gap-filling available in my lab here in beautiful Snowdonia, between July 2025 to end Nov 2026. Generous travel budget. Lab is full of friendly and supportive colleagues. Link below, or DM me/email c.staples@bangor.ac.uk for info

Different Ross Chapman, but glad you enjoyed your meeting 😁

The ageing genome: from mechanisms to disease

Register and submit your abstract now: The ageing genome: from mechanisms to disease www.embl.org/about/info/c...

BRCA1 turned 30 🎉
To celebrate, Jos Jonkers and I explored three decades of BRCA1 research - what we’ve learned about its biology, its role in tumorigenesis and future directions to improve the life of BRCA1 mutation carriers.
Now out in Cancer Discovery ⬇️: aacrjournals.org/cancerdiscov...

The transcriptomic architecture of common cancers reflects synthetic lethal interactions - Nature Genetics Tumor cells upregulate compensatory buffering genes following tumor suppressor loss. These genes may represent new synthetic lethal partners that could be harnessed therapeutically.

We show transcriptomic buffering of tumour suppressor loss via syn. lethal genes is not anecdotal but a cancer hallmark. Buffering also seen in BRCAness, predicts penetrant syn leth effects and outcome. @icr.ac.uk @cancerresearchuk.org @breastcancernow.bsky.social www.nature.com/articles/s41...

Congrats @thecesarelab.bsky.social and @szmyd-radoslaw.bsky.social. It’s been great to see this work develop, and even better to finally see it out in print! 🥂🍻

Chromosome end protection by RAP1-mediated inhibition of DNA-PK During classical non-homologous end joining (cNHEJ), DNA-dependent protein kinase (DNA-PK) encapsulates free DNA ends, forming a recruitment platform for downstream end-joining factors including Ligas...

Really cool work, demonstrating TRF2-RAP1 mediated inhibition of the NHEJ machinery at chromosome ends!

www.biorxiv.org/content/10.1...

Few better ways to end the year with the team than over a few pints (& mini Guinness’s) in the @StarPubOxford

Blskeet 🍪

In our first skeet, check out a very cool postdoc opportunity, in the very cool @susanagodinho.bsky.social lab 👇

Nice to see you on here @oxfordcancer.bsky.social - pls sign me up!

Hi Tatiana - I’ve just joined up! Pls count me in