**Conflict of interest**

The authors do not have any conflicts of interest.

## **Funding**

This study was supported in part by the Lisa Dean Moseley Foundation (BB), Cancer B\*Ware Foundation (BB), and Cawley Center for Translational Cancer Research Fund (BB, CF).

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**Author details**

Delaware, USA

Newark, Delaware, USA

Caroline O.B. Facey1

Research Institute, Newark, Delaware, USA

University, Philadelphia, Pennsylvania, USA

provided the original work is properly cited.

and Bruce M. Boman1,2,3,4\*

2 Department of Biological Sciences, University of Delaware, Newark,

3 Department of Mathematical Sciences, University of Delaware,

\*Address all correspondence to: brucemboman@gmail.com

1 Center for Translational Cancer Research, Helen F. Graham Cancer Center and

4 Department of Pharmacology and Experimental Therapeutics, Thomas Jefferson

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

*Retinoids in Treatment of Colorectal Cancer DOI: http://dx.doi.org/10.5772/intechopen.93699* *Retinoids in Treatment of Colorectal Cancer DOI: http://dx.doi.org/10.5772/intechopen.93699*

*Colorectal Cancer*

**8. Conclusion and future perspectives**

how new SC-targeted therapies might be designed for CRC.

The authors do not have any conflicts of interest.

**8.1 Materials and methods**

proteinatlas.org).

**Funding**

**Conflict of interest**

Research Fund (BB, CF).

Our results indicate that RA signaling, when dysregulated, plays a major role in the SC origin of CRC. Overall, our review provides a strong rationale for future exploration of retinoid therapies for CRC in precision oncology. A few clues gleaned from our review are as follows: (i) drug screens using CRC cell lines (**Table 1**) and knockout of RA-signaling genes in human CRC cells might identify which retinoid drugs are active against cells with specific mutations; (ii) *Apc*Min/+ mice may be useful to identify additional retinoid agents that are active against *Apc* mutant tissues; (iii) strategies for designing retinoid-based CRC therapies will likely need to incorporate retinoids into drug combination regimens; (4) CRCs will likely need to be genotyped to determine the status of RA signaling genes when administering RA-based treatments to CRC patients. Finally, continued discovery of the mechanisms that explain how RA signaling regulate normal colon SCs and how dysregulation of RA signaling in cancer SCs drive CRC growth should provide insight into

The bioinformatics analysis on overexpression and mutation of RA signaling component genes in CRCs was done through the COSMIC website (cancer.sanger. ac.uk/cosmic). Bioinformatics analysis to identify RA signaling genes that predict CRC patient survival was done through The Human Protein Atlas (https://www.

This study was supported in part by the Lisa Dean Moseley Foundation (BB), Cancer B\*Ware Foundation (BB), and Cawley Center for Translational Cancer

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