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Page 990 Lee et al. Cancer Drug Resist 2020;3:980-91 I http://dx.doi.org/10.20517/cdr.2020.73

overexpression, which may contribute to their observed innate resistance to prexasertib [8,16,30,31] . In 2017,
[16]
Lee et al. noted the complex molecular interactions of the RAS/RAF/MEK/ERK pathways with CHK1
inhibitor sensitivity. The data presented here support EGFR as a biomarker for the use of prexasertib and
potentially other CHK1 inhibitors.

DECLARATIONS
Acknowledgments
The authors would like to acknowledge Drs. Jonathan Scammell and Yulia Maxuitenko for their advice and
assistance with animal randomization and data review.

Authors’ contributions
Made substantial contributions to conception and design of the study and performed data analysis and
interpretation: Lee KJ, Schuler M, Gassman NR
Performed data acquisition, as well as provided technical support: Lee KJ, Wright G, Bryant H, Wiggins
LA, Schuler M, Gassman NR
Draft writing and provided material support: Lee KJ, Schuler M, Gassman NR

Availability of data and materials
Data and materials described in this manuscript can be made available upon request.

Financial support and sponsorship
This work was supported by an Innovation Award from the Breast Cancer Research Foundation of Alabama
to MS and NRG (www.brcaf.org). GW is supported by a pre-doctoral fellowship through the University
of South Alabama College of Medicine. The funders played no role in the experiment design, collection,
analysis and interpretation of data, and writing of the manuscript.

Conflicts of interest
All authors declared that there are no conflicts of interest.

Ethical approval and consent to participate
Animal studies were approved by the Institutional Animal Care and Use Committee (IACUC) at the
University of South Alabama.

Consent for publication
Not applicable

Copyright
© The Author(s) 2020.

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