Ontology highlight
ABSTRACT: Background
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) control lung cancer in patients with EGFR mutations, but resistance develops over time. Patients with high levels of genetic mutations rapidly acquire EGFR-TKI resistance. T cell immunity recognizes gene mutation products as neoantigens that effectively suppress mutation levels by eliminating clones with more mutations; this process is known as cancer immune editing. Therefore, EGFR-TKI-resistant clones may be less likely to form in cases with active antitumor T cell immune responses. However, the relationship between EGFR-TKI resistance and antitumor T cell response in patients with EGFR mutation remains unclear. To determine the relationship between the duration of EGFR-TKI resistance acquisition a
SUBMITTER: Mouri A
PROVIDER: S-EPMC12255592 | biostudies-literature | 2025 Jul
REPOSITORIES: biostudies-literature