Craig Anderson

Craig Anderson

@craigandersn.bsky.social

Interested in DNA damage, mutations, adaptation and evolution. DKTK, DKFZ, LMU https://dktk.dkfz.de/en/research/dktk-researchers/anderson-group Munich, Germany

208 followers204 following93 posts

Craig Anderson reposted

How long after a mutation does it take for a cell to progress to cancer? In Barrett’s oesophagus, we found that CNAs occurred decades prior to cancer diagnosis, and that their rate is more prognostic than CNA burden alone doi.org/10.64898/202... (1/6)

Craig Anderson reposted

Craig Anderson reposted

Last week to apply for this. If you are interested in working on cool project to understand the role of DNA methylation in regulating transcription please apply!

Duncan Sproul@sproullab.bsky.social

🚨 #Postdoc position open. Want to understand non-canonical #epigenetic regulation of mammalian transcription? Come work @uoe-igc.bsky.social in Edinburgh! We’re looking for a motivated & collaborative colleague with a strong track record. 📅 14 October 2026 📢 Please share Apply here 👇

Craig Anderson reposted

Check out our latest, just out in @MolecularCell! We reveal how common, typically harmless forms of DNA damage synergise with DNA replication defects in ATM-deficient cells to drive tumour-specific responses to PARP inhibitors - We propose that a similar synergy may contribute to A-T pathogenesis.

Craig Anderson reposted

Craig Anderson reposted

Deadline fast approaching for the Transcription and Chromatin UK meeting - 18-20 November 2026. Submit your abstract for this exciting meeting by tomorrow for a chance to present. Hope to see you in York! 🧬

Lorraine Reese@lorraine-reese.bsky.social

Transcription and Chromatin UK brings together the rich transcription and epigenetics community in the UK and leading experts from abroad. Most talks will be selected from abstracts and interspersed with invited speaker presentations, submit your abstract before 18 Sept! 🧪 bit.ly/4eWyTmc

Craig Anderson reposted

1/ NEW PAPER 🎉 🧵 We mapped the mutational processes shaping 959 prostate cancer genomes from the Pan Prostate Cancer Group (PPCG), integrating SBS, ID, CX and complex SV signatures. Eight footprints account for the processes in 85% of cases www.nature.com/articles/s41... @nature.com

nature.comIntegrated signatures define mutational processes in prostate cancer - NatureEight integrated mutational footprints collectively explain the mutational processes in 85% of primary prostate cancer genomes.

Craig Anderson reposted

Craig Anderson reposted

Craig Anderson reposted

How long does DNA damage last? @aaronquinlan.bsky.social and I found evidence that lesions are transmitted from parent (P0) to offspring (F1) in C. elegans. If they segregate unrepaired for multiple cell divisions, lesions generate multi-allelism in the F1 germline. www.biorxiv.org/content/10.6...

biorxiv.orgInherited DNA damage generates multi-allelic mutations in C. elegansExogenous and endogenous mutagens generate a wide variety of DNA lesions, including bulky adducts, chemical modifications, and single- or double-stranded breaks. A phenomenon called “lesion segregation,” in which lesions evade repair and persist for multiple cell divisions, has recently been documented in tumors and healthy somatic tissues from mice and humans, respectively. Persistent lesions can generate multi-allelic variants (MAVs) by serving as templates for multiple rounds of error-prone replication. By reanalyzing data from a large C. elegans mutagenesis experiment, we observed robust evidence for MAVs at a small fraction (∼0.2%) of mutated sites in the offspring of strains treated with alkylating agents. Because these sequencing data were derived from the progeny of a single F1 animal — itself the offspring of a mutagenized P0 — all mutations should be biallelic. The presence of multi-allelic variation implies that some DNA lesions are transmitted to the F1 zygote, evade repair, and are repeatedly bypassed by error-prone polymerases during embryogenesis. We suspect that many more lesions are inherited than is suggested by MAV prevalence, and that a large fraction of biallelic mutations are also caused by inherited lesions. Our results demonstrate that DNA lesions serve as durable, transgenerational templates for mutagenesis in C. elegans . We speculate that lesion segregation in the early embryo may be a source of mosaicism and genetic diversity in humans, as well. ### Competing Interest Statement The authors have declared no competing interest. National Institutes of Health, https://ror.org/01cwqze88, R01HG012252

Craig Anderson reposted

Craig Anderson reposted

An exciting scientific collaboration 🧪 uncovered a gene–environment "collaboration" in colorectal cancer: an inherited MGMT variant predisposes tumors to alkylating DNA damage, red-meat intake amplifies it—and the damage it causes drives oncogenic KRAS mutations. #EvoDevo doi.org/10.1158/1055...

doi.orgGermline Predisposition to Oncogenic Alkylating Damage in Colorectal CancerAbstractBackground:. Red meat consumption is a risk factor for colorectal cancer and has been linked to tumor alkylating DNA damage. rs16906252-T is a cis expression quantitative trait locus variant a...

Craig Anderson reposted

Check it now! 💫 Exited to share this preprint, the result of a fantastic collaboration between Sarah Aitken’s and Martin Taylor’s labs. During my secondment at @yalecancer.bsky.social @yalepathology.bsky.social, I contributed to explore how H&E images can be used to predict tumour genomics

Sarah Aitken@s-j-aitken.bsky.social

🔬NEW PREPRINT🔬 Explainable machine learning relates histological to genomic pathology www.biorxiv.org/content/10.6... From John Connelly and Barbara Hernando @bhernando.bsky.social, co-led with Martin Taylor @mstaylor.bsky.social - along with others from #LCEConsortium #genomicPathology #ml #ai

Craig Anderson reposted

Accurate detection of somatic mutations is essential for studying mosaicism. This protocol describes CompDuplex-seq, a duplex sequencing method that combines genome-wide coverage with high accuracy using standard Illumina sequencing workflows. Learn more: www.protocols.io/view/compdup...

protocols.ioCompDuplex: Accurate detection of somatic mutations by duplex-seq with comprehensive genome coverageCompDuplex: Accurate detection of somatic mutations by duplex-seq with comprehensive genome coverage. . Read full protocol, steps, and materials on protocols.io

Craig Anderson reposted

In a new (ish) preprint, we used CRISPR barcodes to label germline stem cell clones in zebrafish, then tracked their contributions to sperm production for 2 years. Instead of staying stable, individual clones rose, fell, and disappeared over time. www.biorxiv.org/content/10.6...

biorxiv.orgClonal dynamics deviate from neutral drift in zebrafish spermatogenesisSpermatogonial stem cells (SSCs) maintain male fertility, but how their clonal dynamics change with age remains poorly understood. Here, we use in vivo CRISPR barcoding in zebrafish to label SSCs and ...

Craig Anderson reposted

Craig Anderson reposted

Craig Anderson reposted

🧬NEW PAPER🧬 To what extent is cancer development deterministic? Does the germline genome affect that predictability? Find out in our #StrainDifferences paper @nature.com "Genetic background sets the trajectory of experimental cancer evolution" www.nature.com/articles/s41... 🧵[1/14]

nature.comGenetic background sets the trajectory of experimental cancer evolution - NatureExperimentally replaying tumour evolution in divergent mouse strains reveals the importance of interactions between genetic ancestry and acquired cancer-driving mutations in shaping the earliest stage...

Craig Anderson reposted

Craig Anderson reposted

What if DNA methylation changes aren’t just ticking of our biological clock but rather the rust breaking the gears? Very excited to share our work - how DNA methylation contributes to stem cell dysfunction and aging, published in @natgenet.nature.com doi.org/10.1038/s415... #epigenetics #aging 1/11

doi.orgA progeria syndrome links DNA hypermethylation to age-related pathology - Nature GeneticsThis study investigates the consequences of hypermethylation in a progeria syndrome caused by gain-of-function DNMT3A mutations, finding effects on adult stem cell function.

Craig Anderson reposted

Craig Anderson reposted

Craig Anderson reposted

Craig Anderson reposted

A gene is recurrently mutated in cancer. But do these mutations really cause the disease? Or are they merely selected during normal tissue evolution? Postdoc D. Cheek had the creative idea to use patient ages to try and answer this question. Read new paper out here: www.nature.com/articles/s41...

nature.comAge distinguishes selection from causation in cancer genomes - Nature GeneticsMutations may be enriched in tumor samples because they promote carcinogenesis or because they promote clonal expansions in healthy tissue. This study mathematically disentangles these two possibiliti...

Craig Anderson reposted

Excited to share our latest work in Nature. Applying single-molecule and single-cell DNA sequencing methods, we uncover an extraordinary landscape of somatic mutations in immune checkpoint genes in autoimmune B cells, suggesting that somatic mutations may be key to autoimmunity [1/n] rdcu.be/fdqbr

rdcu.bePolyclonal selection of immune checkpoint mutations in thyroid autoimmunityNature - Polyclonal selection of immune checkpoint mutations in thyroid autoimmunity