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ABSTRACT: Introduction
EGFR-mutant lung cancers are clinically and genomically heterogeneous with concurrent RB transcriptional corepressor 1 (RB1)/tumor protein p53 (TP53) alterations identifying a subset at increased risk for small cell transformation. The genomic alterations that induce lineage plasticity are unknown.Methods
Patients with EGFR/RB1/TP53-mutant lung cancers, identified by next-generation sequencing from 2014 to 2018, were compared to patients with untreated, metastatic EGFR-mutant lung cancers without both RB1 and TP53 alterations. Time to EGFR-tyrosine kinase inhibitor discontinuation, overall survival, SCLC transformation rate, and genomic alterations were evaluated.Results
Patients with EGFR/RB1/TP53-mutant lung cancers represented 5% (43 of 863) of EGFR-
SUBMITTER: Offin M
PROVIDER: S-EPMC6764905 | biostudies-literature | 2019 Oct
REPOSITORIES: biostudies-literature