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• W3159018105 abstract "Proteogenomic evolution of metastatic tumors results in tumor heterogeneity that influences treatment response and overall prognosis. Here, we perform whole-exome and transcriptome sequencing, SNP array for copy number alterations (CNA) and mass spectrometry-based quantitative proteomics of lung adenocarcinoma (LUAD) and thymic carcinoma (TC) metastases obtained by rapid autopsy to elucidate mechanisms of tumor heterogeneity. APOBEC-mutagenesis driven by APOBEC3 region transcripts strongly correlated with mutational tumor heterogeneity. TP53 mutation status was associated with APOBEC hypermutator status. Interferon pathways were enriched in tumors with high APOBEC mutagenesis. Furthermore, interferon treatment of LUAD cells or immortalized lung epithelial cells in culture upregulated APOBEC3 region transcripts, suggesting a role for the immune microenvironment in the generation of mutational heterogeneity. CNA occurring late in tumor evolution correlated with downstream transcriptomic and proteomic heterogeneity between metastases. These results illustrate key mechanisms underlying multi-dimensional heterogeneity in metastatic thoracic tumors." @default.
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• W3159018105 date "2018-01-01" @default.
• W3159018105 modified "2023-10-18" @default.
• W3159018105 title "APOBEC Mutagenesis and Copy Number Alterations are Drivers of Proteogenomic Tumor Evolution and Heterogeneity in Metastatic Thoracic Tumors" @default.
• W3159018105 doi "https://doi.org/10.2139/ssrn.3215351" @default.
• W3159018105 hasPublicationYear "2018" @default.
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