Missed it? Our March preprint shows how endogenous oxidative base damage drives the PARPi response in ATM-deficient cells. In working this out we uncovered a role for ATM in safeguarding replication through damaged DNA and discuss what this could mean for Ataxia-Telangiectasia.

MRC Weatherall Institute of Molecular Medicine@imm.ox.ac.uk · 3w ago

#WIMMReads🧪 From the Chapman Group: a new preprint offers a potential explanation for why ATM deficient cancers respond to PARP inhibitors, with implications for cancer treatment and Ataxia Telangiectasia. #CancerResearch #AcademicSky @rdm.ox.ac.uk @medsci.ox.ac.uk @rosschapmanlab.bsky.social 🧬

#WIMMReads🧪 From the Chapman Group: a new preprint offers a potential explanation for why ATM deficient cancers respond to PARP inhibitors, with implications for cancer treatment and Ataxia Telangiectasia. #CancerResearch #AcademicSky @rdm.ox.ac.uk @medsci.ox.ac.uk @rosschapmanlab.bsky.social 🧬

ATM safeguards DNA replication at endogenous base lesions

Poly(ADP-ribose) polymerase inhibitors (PARPi) exploit homologous recombination deficiency (HRD) in BRCA1/2-mutated cancers to induce synthetic lethality[1][1]–[3][2]. PARPi also kill cancer cells lac...

doi.org

Still contemplating joining us at EMBO-DDR 2026 this October? We have a stellar lineup with slots for short talks (selected from abstracts) still up for grabs. EMBO have extended the registration/abstract deadline until 29 May to accommodate new registration requests! See you (in) Sounio 😎🧬🇬🇷!

Still contemplating joining us at EMBO-DDR 2026 this October? Many slots for short talks (selected from abstracts) are still up for grabs and EMBO have extended the registration/abstract deadline until 20 May 23:59:59 CET to accommodate some late registration requests- Hope to see many of you there!

Ross Chapman@rosschapmanlab.bsky.social · 4mo ago

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!

Great conference, great science and great location!

Ross Chapman@rosschapmanlab.bsky.social · 4mo ago

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!

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!

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...

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...

jobs.icr.ac.uk

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...

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...

biorxiv.org

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

Ross Chapman@rosschapmanlab.bsky.social · 8mo ago

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...

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...

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...

biorxiv.org

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

James Davies@jojdavies.bsky.social · 9mo ago

Our latest paper has just been published in Cell! doi.org/10.1016/j.ce... We developed a new method called MCC ultra, which allows 3D chromatin structure to be visualised with a 1 base pair pixel size.

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...

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.

fast.wistia.com

Congrats Kelly! 🥂

MRC Laboratory of Molecular Biology@mrclmb.ac.uk · last yr.

Congratulations to @kellythd-nguyen.bsky.social, Group Leader in the LMB’s Structural Studies Division, who has been awarded the 2025 Research Prize from @thelisterinstitute.bsky.social . Read more here: www2.mrc-lmb.cam.ac.uk/kelly-nguyen... #LMBNews

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...

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...

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.

bbc.com

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

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

The ageing genome: from mechanisms to disease

embl.org

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...

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...

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.

nature.com

Really cool work, demonstrating TRF2-RAP1 mediated inhibition of the NHEJ machinery at chromosome ends! www.biorxiv.org/content/10.1...

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...

biorxiv.org

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

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

Susana Godinho@susanagodinho.bsky.social · 2y ago

We have a very cool (I know I am biased😁) project for a computational biologist (postdoc) interested in cancer evolution in collaboration with Nicky McGranahan’s lab! Perfect opportunity to expand your computational skills too! 👉 www.godinholab.com RT please 🙏🙏🙏👍👍