Anti-EGFR-resistant clones decay exponentially after progression: implications for anti-EGFR re-challenge.

ABSTRACT:

Background

Colorectal cancer (CRC) has been shown to acquire RAS and EGFR ectodomain mutations as mechanisms of resistance to epidermal growth factor receptor (EGFR) inhibition (anti-EGFR). After anti-EGFR withdrawal, RAS and EGFR mutant clones lack a growth advantage relative to other clones and decay; however, the kinetics of decay remain unclear. We sought to determine the kinetics of acquired RAS/EGFR mutations after discontinuation of anti-EGFR therapy.

Patients and methods

We present the post-progression circulating tumor DNA (ctDNA) profiles of 135 patients with RAS/BRAF wild-type metastatic CRC treated with anti-EGFR who acquired RAS and/or EGFR mutations during therapy. Our validation cohort consisted of an external dataset of 73 patients with a ctDNA profile sugges

SUBMITTER: Parseghian CM 

PROVIDER: S-EPMC6657008 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature