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Re-challenge of Anti-EGFR for Patients With RAS/BRAF Wild-type Metastatic CRC

ABSTRACT: The aim of the trial is to study the efficacy and safety of Cetuximab re-challenge for Chinese Patients with RAS/BRAF wild-type Metastatic Colorectal Cancer.

DISEASE(S): Metastatic Colorectal Cancer,Colorectal Neoplasms

PROVIDER: 2326638 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Cetuximab Re-challenge for Colorectal Cancer Liver Metastasis

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Anti-BRAF mutation drug resistance enhances EGFR expression in melanomas [expression profiling]

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Anti-BRAF mutation drug resistance enhances EGFR expression in melanomas [methylation profiling]

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

Project description:BackgroundColorectal 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 methodsWe 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 suggestive of prior anti-EGFR exposure and serial sampling. A separate retrospective cohort of 80 patients was used to evaluate overall response rate and progression free survival during re-challenge therapies.ResultsOur analysis showed that RAS and EGFR relative mutant allele frequency decays exponentially (r2=0.93 for RAS; r2=0.94 for EGFR) with a cumulative half-life of 4.4 months. We validated our findings using an external dataset of 73 patients with a ctDNA profile suggestive of prior anti-EGFR exposure and serial sampling, confirming exponential decay with an estimated half-life of 4.3 months. A separate retrospective cohort of 80 patients showed that patients had a higher overall response rate during re-challenge therapies after increasing time intervals, as predicted by our model.ConclusionThese results provide scientific support for anti-EGFR re-challenge and guide the optimal timing of re-challenge initiation.

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Mpox infection protects against re-challenge in rhesus macaques

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