1/7 4️⃣ novel #mutationalsignatures confirmed using SigProfilerExtractor (SPE) & in COSMIC now🧬Find out about SPE & how these were discovered in the article linked below, or follow the handy guide in this thread🧵Cell Genomics Wellcome Sanger Institute Cancer Grand Challenges bit.ly/3DOildT

The first virology paper from the lab!!! We discovered that APOBEC3B regulates the innate immune system, promoting translation blockage and protecting stress granules from RNase L during RNA viral infections, independently of its deaminase activity. nature.com/articles/s4146…

🚨 ONLINE Nature Genetics 📰 Multiomic analysis of malignant pleural #mesothelioma identifies molecular axes and specialized tumor profiles driving intertumor heterogeneity 👩🏾‍🤝‍👨🏻Mangiante @FCLynnette IARC Rare Cancers Genomics and team 👇🏻 go.nature.com/3JKD6JX

So when does ecDNA arise, exactly? Our study on #ecDNA and the transformation of pre-cancerous Barrett’s esophagus into cancer is out today. This collaboration brought together @Team_eDyNAmiC, Rebecca Fitzgerald Lab and the @FredHutch Seattle Barrett’s Study.🧵 nature.com/articles/s4158…

Pre-print alert 🚨Excited to share our new preprint “The interplay between mutagenesis and extrachromosomal DNA shapes urothelial cancer evolution” 🧬🔬#bladdercancer bit.ly/3B3S2hi OncoAlert

A3A Spurs Evolution of Drug-Tolerant Persister Cells in Response to Targeted Therapies. Kudos to Hideko Isozaki from Aaron Hata's lab. Delighted to have contributed to this first study demonstrating the role of A3A in promoting drug resistance. nature.com/articles/s4158…

Our research is published in Cell Reports. Topography of mutational signatures in human cancer: Cell Reports cell.com/cell-reports/f…

We are live NYU Grossman School of Medicine ! petljaklab.com 🧫💻 Looking for exper. & comp. staff,postdocs,trainees 🧬 To delve w us into the somatic mosaicism in cancer & aging 🌇 In CURE facilities in the heart of Manhattan cure.345pas.com 📧 [email protected]

Bioengineers UC San Diego have unearthed a connection between the genome's structure & cancer mutations. Just as Earth's diverse terrains foster distinct ecosystems, certain regions in the genome (due to their topographic features) act as mutation hotspots. today.ucsd.edu/story/topograp…

Happy to have been part of this project led by Agnese Cristini in the Gromak Lab and Jennifer L. McCann from The Harris Lab investigating the novel role of APOBEC3B in R-loop regulation and its contribution to R-loop mutagenesis in cancer Nature Genetics nature.com/articles/s4158…

Beautiful review article on ecDNA in Nature Reviews Cancer by Howard Chang Mischel Lab !! 🔥🔥👇🏻👇🏻 nature.com/articles/s4156…

Now online! APOBEC3A and APOBEC3B drive distinct mutational landscapes in tumors. We showed how A3A and A3B substrate preferences for different hairpin structures can be exploited to identify patients' tumors with mutations caused by either A3A or A3B. nature.com/articles/s4146…

And thanks to the brilliant Cancer Grand Challenges team at CRUK for their total support since Mutographs started, as well as wonderful scientific journey with Wellcome Sanger Institute and UC San Diego colleagues (esp Sarah Moody), partners in the 11 countries, and all the great team IARC.

How to improve effectiveness of cancer immunotherapy? Integrate multiple layers of omic data with #AI nature.com/articles/s4301… Nature Cancer

An approach using multi-omics data & machine learning to improve patient selection for ICB (immune checkpoint blockade) therapy, offering more effective treatment wrote the authors in @naturecancer paper. By ErikBergstrom & Ludmil Alexandrov of @ucsandiego

Our new paper published today in nature! Study Uncovers Mutations and DNA Structures Driving Bladder Cancer news.weill.cornell.edu/news/2024/10/s…

How does cancer therapy affect extrachromosmal DNA status? Take a look at this illuminating work from Hoon Kim and Roel Verhaak and their teams. Want to view and explore our ecDNA predictions from TCGA & PCAWG? We've shared them publicly: ampliconrepository.org

Now online in Cancer Discovery: Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage - by Yun Rose Li, Allan Balmain, and colleagues doi.org/10.1158/2159-8… City of Hope UC San Francisco