Abstract
In recent decades, survival rates in colorectal cancer have improved greatly due to pharmacological treatment. However, many patients end up developing adverse drug reactions that can be severe or even life threatening, and that affect their quality of life. These remain a limitation, as they may force dose reduction or treatment discontinuation, diminishing treatment efficacy. From candidate gene approaches to genome-wide analysis, pharmacogenomic knowledge has advanced greatly, yet there is still huge and unexploited potential in the use of novel technologies such as next-generation sequencing strategies. This review summarises the road of colorectal cancer pharmacogenomics so far, presents considerations and directions to be taken for further works and discusses the path towards implementation into clinical practice.
Highlights
Colorectal cancer (CRC) is the second leading cause of cancer-related death and the third most commonly diagnosed cancer [1]
Metastatic CRC treatment may in addition include biological targeted agents to improve patient outcome, such as monoclonal antibodies against vascular endothelial growth factor (VEGF), or against epidermal growth factor receptor (EGFR) (Table 1) [4]
This might be explained by a work of Rosmarin et al in 2015, which reported an association of an intronic variant located in the overlapping ENOSF1 gene capable of explaining the toxicity attributed to the two previous Thymidylate Synthetase (TYMS) polymorphisms
Summary
Colorectal cancer (CRC) is the second leading cause of cancer-related death and the third most commonly diagnosed cancer [1]. The first line of treatment is based on fluoropyrimidines: 5-fluorouracil (5-FU) or its oral prodrug capecitabine, either alone or in different combinations with other agents, the most common being leucovorin, oxaliplatin (named FOLFOX or XELOX -if capecitabine is used instead of 5FU) or irinotecan (FOLFIRI) [2,3,4,5] Besides these cytotoxic agents, metastatic CRC (mCRC) treatment may in addition include biological targeted agents to improve patient outcome, such as monoclonal antibodies against vascular endothelial growth factor (VEGF) (bevacizumab), or against epidermal growth factor receptor (EGFR) (cetuximab and panitumumab) (Table 1) [4]. We discuss considerations for further studies towards a routine implementation of personalised medicine strategies in clinical practice
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