Abstract

Despite the use of standard adjuvant treatment (ACT) based on fluoropyrimidines plus oxaliplatin, up to 80% of patients with localized colorectal cancer (CC) presents detectable circulating tumor DNA (ctDNA) related with relapse. No biomarkers of response and resistance to ACT have been clarified and the molecular mechanisms of relapse remain unknown. Our aim is to identify the dynamic molecular changes at relapse, intratumoral heterogeneity (ITH) and potential novel therapeutic approaches to eradicate residual disease.

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