A compendium of mutational signatures of environmental agents. An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers. Mutational signature SBS8 predominantly arises due to late replication errors in cancer. Deficiency of nucleotide excision repair is associated with mutational signature observed in cancer. Characterizing mutational signatures in human cancer cell lines reveals episodic APOBEC mutagenesis. SigProfilerMatrixGenerator: a tool for visualizing and exploring patterns of small mutational events. The repertoire of mutational signatures in human cancer. ![]() Whole-genome sequencing of triple-negative breast cancers in a population-based clinical study. Pathogenic germline variants in 10,389 adult cancers. A compendium of mutational cancer driver genes. Ubiquitin-activating enzyme UBA1 is required for cellular response to DNA damage. Comprehensive characterization of cancer driver genes and mutations. Allele-specific HLA loss and immune escape in lung cancer evolution. Mitochondrial DNA copy number variation across human cancers. Selective and mechanistic sources of recurrent rearrangements across the cancer genome. Co-occurring genomic alterations define major subsets of KRAS-mutant lung adenocarcinoma with distinct biology, immune profiles, and therapeutic vulnerabilities. Tracing lung cancer risk factors through mutational signatures in never smokers: the Sherlock-Lung study. Whole-genome characterization of lung adenocarcinomas lacking the RTK/RAS/RAF pathway. Frequent alterations in cytoskeleton remodelling genes in primary and metastatic lung adenocarcinomas. Frequent mutations in chromatin-remodelling genes in pulmonary carcinoids. Whole-genome sequencing reveals genomic signatures associated with the inflammatory microenvironments in Chinese NSCLC patients. Somatic genomics and clinical features of lung adenocarcinoma: a retrospective study. Tracing oncogene rearrangements in the mutational history of lung adenocarcinoma. Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing. Genomic landscape of non-small cell lung cancer in smokers and never-smokers. Genomic landscape of lung adenocarcinoma in East Asians. Comprehensive molecular profiling of lung adenocarcinoma. Distinct patterns of somatic genome alterations in lung adenocarcinomas and squamous cell carcinomas. Proportion and clinical features of never-smokers with non-small cell lung cancer. The Cancer Atlas: Lung Cancer (American Cancer Society, 2021) Ĭho, J. These findings create avenues for personalized treatment in LCINS. Genes within the receptor tyrosine kinase–Ras pathway had distinct impacts on survival five genomic alterations independently doubled mortality. No strong tobacco smoking signatures were detected, even in cases with exposure to secondhand tobacco smoke. The other subtypes are characterized by specific amplifications and EGFR mutations (mezzo-forte) and whole-genome doubling (forte). The dominant subtype (piano), which is rare in lung cancer in smokers, features somatic UBA1 mutations, germline AR variants and stem cell-like properties, including low mutational burden, high intratumor heterogeneity, long telomeres, frequent KRAS mutations and slow growth, as suggested by the occurrence of cancer drivers’ progenitor cells many years before tumor diagnosis. ![]() Here high-coverage whole-genome sequencing of 232 LCINS showed 3 subtypes defined by copy number aberrations. Lung cancer in never smokers (LCINS) is a common cause of cancer mortality but its genomic landscape is poorly characterized. Nature Genetics volume 53, pages 1348–1359 ( 2021) Cite this article Genomic and evolutionary classification of lung cancer in never smokers
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