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Review
. 2016 Jul;8(4):276-93.
doi: 10.1177/1758834016646734. Epub 2016 May 29.

Current targeted therapies in the treatment of advanced colorectal cancer: a review

Andrew Moriarity  1 , Jacintha O'Sullivan  2 , John Kennedy  2 , Brian Mehigan  2 , Paul McCormick  2
Affiliations
Review

Current targeted therapies in the treatment of advanced colorectal cancer: a review

Andrew Moriarity et al. Ther Adv Med Oncol. 2016 Jul.

Abstract

Treatment strategies for metastatic colorectal cancer (mCRC) patients have undergone dramatic changes in the past decade and despite improved patient outcomes, there still exist areas for continued development. The introduction of targeted agents has provided clinicians with additional treatment options in mCRC, however, results have been mixed at best. These novel therapies were designed to interfere with specific molecules involved in the cellular carcinogenesis pathway and ultimately deliver a more focused treatment. Currently, their use in mCRC has been limited primarily as an adjunct to conventional chemotherapy regimens. This review explores the relevant cell-signaling networks in colorectal cancer, provides focus on the current targeted agent armamentarium approved for use in mCRC and explores the usefulness of predictive mCRC biomarkers.

Keywords: biomarkers; colorectal cancer; signaling; targeted therapy.

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Conflict of interest statement

Conflict of interest statement: The author(s) declared that there is no conflict of interest.

Figures

Figure 1.
Figure 1.
Schematic of an endothelial cell depicting VEGFR-1, VEGFR-2, and VEGFR-3 and the mechanisms of action of the antiangiogenic agents bevacizumab, aflibercept, ramucirumab and regorafenib. Bevacizumab and aflibercept bind to VEGF and interrupt the interaction with VEGF receptors. Regorafenib is a small-molecule multi-kinase inhibitor of which targets include VEGFR-1 and VEGFR-3. TAS-102 consists of trifluridine that is incorporated into DNA, inducing DNA dysfunction, including DNA strand breakage. Cetuximab and panitumumab are anti-EGFR treatments that result in disruption of the MAP kinase pathway. EGFR, endothelial growth-factor receptor; VEGF, vascular endothelial growth factor; VEGFR, vascular endothelial growth-factor receptor; DNA, deoxyribonucleic acid; MAP, a protein kinase signaling pathway.
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