Abstract
Abstract Colorectal cancers evolve by a reiterative process of genetic diversification and clonal evolution. Tissue and liquid biopsies can be used to define CRC molecular subtypes and to monitor clonal evolution during therapy. Using these approaches, CRC patients were found to respond selectively to targeted agents interfering with oncogenic nodes of the EGFR signaling pathway. Notably, the patient-specific responses can be recapitulated and paralleled in cellular and mouse clinical proxies (CRC-avatars). The inevitable development of acquired resistance to inhibitors of the EGFR signaling axis presently limits further clinical advances. Strategies to prevent or overcome resistance are therefore essential to design the next generation of molecularly-driven clinical trials for CRC patients. Citation Format: Alberto Bardelli. Heterogeneity, drug resistance, and clonal dynamics in colorectal cancers. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl 2):Abstract nr CN02-03.
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