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Evolution and clinical impact of genetic epistasis within EGFR-mutant lung cancersDOI 10.1101/117291
Tobacco smoke alters the trajectory of lung adenocarcinoma evolution via effects on somatic selection and epistasisSemantic proximity
Oncogenic context shapes the fitness landscape of tumor suppressionSemantic proximity
Oncogenic context shapes the fitness landscape of tumor suppression.Semantic proximity
Epistatic interactions and drug response.Semantic proximity
Genetic background sets the trajectory of cancer evolutionSemantic proximity
Germline mutations and developmental mosaicism underlying<i>EGFR</i>-mutant lung cancerSemantic proximity
Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers.Semantic proximity
EGFR and ERBB2 Germline Mutations in Chinese Lung Cancer Patients and Their Roles in Genetic Susceptibility to CancerSemantic proximity
Genetic Determinants of EGFR-Driven Lung Cancer Growth and Therapeutic Response In VivoSemantic proximity
Synergistic epistasis among cancer drivers can rescue early tumors from the accumulation of deleterious passengers.Semantic proximity
Cancer type-dependent genetic interactions between cancer driver alterations indicate plasticity of epistasis across cell types.Semantic proximity
Mutational landscape of EGFR-, MYC-, and Kras-driven genetically engineered mouse models of lung adenocarcinoma.Semantic proximity
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