Early life exposure to N-nitrosamine drives genotoxicity, mutagenesis, and tumorigenesis in DNA repair-deficient mice

# Data and Code Repository for Volk et al., 2025 This repository contains the source code for **Volk et al., 2025, Nature Communications**. ## Project Overview This study investigates the age-dependent susceptibility to liver carcinogenesis induced by N-Nitrosodimethylamine (NDMA). The project integrates multiple genomic and imaging approaches to understand why juvenile mice are significantly more susceptible to NDMA-induced tumors compared to adults. ### Key Data Types The manuscript includes data from four primary experimental approaches: 1. **[Genomics (Duplex Sequencing)]** * **Goal**: To measure mutagenesis with ultra-high accuracy. * **Data**: Mutation frequencies and mutational spectra analysis comparing NDMA-treated and control mice across age groups. 2. **Transcriptomics (RNAseq)** * **Goal**: To identify differentially expressed genes and dysregulated pathways. * **Data**: Gene expression profiles focusing on inflammation, DNA repair, and interferon response pathways. 3. **Recombination Analysis (RaDR Mice)** * **Goal**: To visualize and quantify homologous recombination events in situ. * **Data**: Fluorescence microscopy images of liver tissue from RaDR (Recombination and DNA Repair) reporter mice, quantifying both punctate foci (DNA damage response) and clonal expansions (mutagenic events). 4. **Tissue Pathology & Imaging** * **Goal**: To assess tissue architecture, DNA damage, and cell proliferation. * **Data**: * **Histopathology**: H&E stained tissue sections for tumor burden and tissue morphology. * **Immunofluorescence**: Staining for DNA damage markers (pH2AX), cell proliferation (Ki67), and DNA replication (BrdU).