<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Manuel Mastel</submitter><organism>Mus musculus</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-17103</full_dataset_link><description>BRAF mutant colorectal cancer displays a unmet clinical need with poor overall survival. Here we modeled this cancer in the murine system with Braf activation mutation, Trp53 deletion and Nicd1 expression. The respective alleles are recombined in the intestinal epithelium upon systemic tamoxifen injection. Tumors were occuring in the small intestine and in the colon. We conducted exon sequencing to investigate if other mutations occur in the tumor development.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sample Collection - Tumor samples and matched normal tissue from the same donor were collected for whole exome sequencing analysis. Genomic DNA was isolated from tumor material and corresponding normal tissue for paired somatic variant calling.</sample_protocol><sample_protocol>Library Construction - Whole exome sequencing libraries were generated using the SureSelectXT Automation Reagent Kit according to the manufacturer’s instructions. Briefly, 200 ng of genomic DNA was fragmented to approximately 150 bp using a Covaris LE220 ultrasonicator. Library preparation was performed on a Bravo automated liquid handler and included end repair, A-tailing, adaptor ligation, and amplification. Library concentration was assessed using the Agilent TapeStation. Subsequently, 750 ng of amplified adaptor-ligated DNA library was hybridized with the SureSelectXT All Exon v7 bait set. DNA-library/bait hybrids were captured using streptavidin-coated magnetic beads. Index tags were added during PCR amplification of the captured libraries. Final libraries were validated using Qubit and Agilent TapeStation.</sample_protocol><sample_protocol>Sequencing - Final whole exome sequencing libraries were sequenced using 2 × 100 bp paired-end sequencing on an Illumina NovaSeq 6000 according to the manufacturer’s protocol.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Genomic DNA was extracted from tumor and matched normal tissue samples. A total of 200 ng gDNA per sample was used for downstream library preparation.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><data_protocol>Data Transformation - Raw sequencing data were aligned to the mouse reference genome using BWA MEM. Somatic SNVs and indels were called with Strelka2 by pairing each mouse tumor sample with matched normal tissue from the same donor. Variants were annotated with SnpEff, and VCF files were filtered to retain only high-confidence variants passing the “PASS” filter. Variant allele frequencies were calculated from the filtered variant calls. Variants located in the selected gene set were extracted and converted into tab-delimited text files for submission.</data_protocol><data_protocol>Sequence Alignment - Whole exome sequencing reads were aligned to the reference genome using BWA-MEM. The resulting aligned datasets were used for downstream SNV and indel calling with Strelka2. For mouse tumors, tumor samples were paired with matched normal tissue from the same donor for somatic mutation calling. Variants were annotated using SnpEff, and VCF files were filtered to retain only high-confidence variants passing the “PASS” filter.</data_protocol><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>exome sequencing</study_type><species>Mus musculus</species><pubmed_authors>Manuel Mastel</pubmed_authors></additional><is_claimable>false</is_claimable><name>Exon sequencing of mouse tails and respective tumors from mice with VBPN genetic background</name><description>BRAF mutant colorectal cancer displays a unmet clinical need with poor overall survival. Here we modeled this cancer in the murine system with Braf activation mutation, Trp53 deletion and Nicd1 expression. The respective alleles are recombined in the intestinal epithelium upon systemic tamoxifen injection. Tumors were occuring in the small intestine and in the colon. We conducted exon sequencing to investigate if other mutations occur in the tumor development.</description><dates><release>2026-06-12T00:00:00Z</release><modification>2026-06-12T01:00:37.057Z</modification><creation>2026-05-20T13:42:27.889Z</creation></dates><accession>E-MTAB-17103</accession><cross_references><ENA>ERP193637</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0005396</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0004917</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003816</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>