REFERENCES
1. Cleary JM, Aguirre AJ, Shapiro GI, D’Andrea AD. Biomarker-guided development of DNA repair inhibitors. Mol Cell 2020;78:1070-85.
2. Ronco C, Martin AR, Demange L, Benhida R. ATM, ATR, CHK1, CHK2 and WEE1 inhibitors in cancer and cancer stem cells. Medchemcomm 2017;8:295-319.
3. Kim H, George E, Ragland R, et al. Targeting the ATR/CHK1 axis with PARP Inhibition results in tumor regression in BRCA-mutant ovarian cancer models. Clin Cancer Res 2017;23:3097-108.
4. Yazinski SA, Comaills V, Buisson R, et al. ATR inhibition disrupts rewired homologous recombination and fork protection pathways in PARP inhibitor-resistant BRCA-deficient cancer cells. Genes Dev 2017;31:318-32.
5. Parmar K, Kochupurakkal BS, Lazaro JB, et al. The CHK1 Inhibitor prexasertib exhibits monotherapy activity in high-grade serous ovarian cancer models and sensitizes to PARP inhibition. Clin Cancer Res 2019;25:6127-40.
6. King C, Diaz HB, McNeely S, et al. LY2606368 causes replication catastrophe and antitumor effects through CHK1-dependent mechanisms. Mol Cancer Ther 2015;14:2004-13.
7. Lee JM, Nair J, Zimmer A, et al. Prexasertib, a cell cycle checkpoint kinase 1 and 2 inhibitor, in BRCA wild-type recurrent high-grade serous ovarian cancer: a first-in-class proof-of-concept phase 2 study. Lancet Oncol 2018;19:207-15.
8. Lowery CD, Dowless M, Renschler M, et al. Broad spectrum activity of the checkpoint kinase 1 inhibitor prexasertib as a single agent or chemopotentiator across a range of preclinical pediatric tumor models. Clin Cancer Res 2019;25:2278-89.
9. Lowery CD, VanWye AB, Dowless M, et al. The checkpoint kinase 1 inhibitor prexasertib induces regression of preclinical models of human neuroblastoma. Clin Cancer Res 2017;23:4354-63.
10. Bryant C, Rawlinson R, Massey AJ. Chk1 inhibition as a novel therapeutic strategy for treating triple-negative breast and ovarian cancers. BMC Cancer 2014;14:570.
11. Choi C, Cho WK, Park S, et al. Checkpoint kinase 1 (CHK1) inhibition enhances the sensitivity of triple-negative breast cancer cells to proton irradiation via Rad51 downregulation. Int J Mol Sci 2020;21:2691.
12. Ma CX, Cai S, Li S, et al. Targeting Chk1 in p53-deficient triple-negative breast cancer is therapeutically beneficial in human-in-mouse tumor models. J Clin Invest 2012;122:1541-52.
13. Mani C, Jonnalagadda S, Lingareddy J, et al. Prexasertib treatment induces homologous recombination deficiency and synergizes with olaparib in triple-negative breast cancer cells. Breast Cancer Res 2019;21:104.
14. Gatti-Mays ME, Karzai FH, Soltani SN, et al. A phase II single arm pilot study of the CHK1 inhibitor prexasertib (LY2606368) in BRCA wild-type, advanced triple-negative breast cancer. Oncologist 2020. doi: 10.1634/theoncologist.2020-0491
15. Booth L, Cruickshanks N, Ridder T, et al. PARP and CHK inhibitors interact to cause DNA damage and cell death in mammary carcinoma cells. Cancer Biol Ther 2013;14:458-65.
16. Lee HJ, Cao Y, Pham V, et al. Ras-MEK signaling mediates a critical Chk1-dependent DNA damage response in cancer cells. Mol Cancer Ther 2017;16:694-704.
17. Gonzalez-Conchas GA, Rodriguez-Romo L, Hernandez-Barajas D, et al. Epidermal growth factor receptor overexpression and outcomes in early breast cancer: a systematic review and a meta-analysis. Cancer Treat Rev 2018;62:1-8.
18. Liu D, He J, Yuan Z, et al. EGFR expression correlates with decreased disease-free survival in triple-negative breast cancer: a retrospective analysis based on a tissue microarray. Med Oncol 2012;29:401-5.
19. Rimawi MF, Shetty PB, Weiss HL, et al. Epidermal growth factor receptor expression in breast cancer association with biologic phenotype and clinical outcomes. Cancer 2010;116:1234-42.
20. Chou TC. Theoretical basis, experimental design, and computerized simulation of synergism and antagonism in drug combination studies. Pharmacol Rev 2006;58:621-81.
21. Sonavane M, Sykora P, Andrews JF, Sobol RW, Gassman NR. Camptothecin efficacy to poison Top1 is altered by bisphenol A in mouse embryonic fibroblasts. Chem Res Toxicol 2018;31:510-9.
22. Yip C, Foidart P, Somja J, et al. MT4-MMP and EGFR expression levels are key biomarkers for breast cancer patient response to chemotherapy and erlotinib. Br J Cancer 2017;116:742-51.
23. Schottle J, Chatterjee S, Volz C, et al. Intermittent high-dose treatment with erlotinib enhances therapeutic efficacy in EGFR-mutant lung cancer. Oncotarget 2015;6:38458-68.
24. She QB, Solit DB, Ye Q, et al. The BAD protein integrates survival signaling by EGFR/MAPK and PI3K/Akt kinase pathways in PTEN-deficient tumor cells. Cancer Cell 2005;8:287-97.
25. Nair J, Huang TT, Murai J, et al. Resistance to the CHK1 inhibitor prexasertib involves functionally distinct CHK1 activities in BRCA wild-type ovarian cancer. Oncogene 2020;39:5520-35.
26. Zeng L, Beggs RR, Cooper TS, Weaver AN, Yang ES. Combining Chk1/2 inhibition with cetuximab and radiation enhances in vitro and in vivo cytotoxicity in head and neck squamous cell carcinoma. Mol Cancer Ther 2017;16:591-600.
27. Park HS, Jang MH, Kim EJ, et al. High EGFR gene copy number predicts poor outcome in triple-negative breast cancer. Modern Pathol 2014;27:1212-22.
28. Matsuo T, Nishizuka SS, Ishida K, et al. Analysis of the anti-tumor effect of cetuximab using protein kinetics and mouse xenograft models. BMC Res Notes 2011;4:140.
29. Kimple RJ, Vaseva AV, Cox AD, et al. Radiosensitization of epidermal growth factor receptor/HER2-positive pancreatic cancer is mediated by inhibition of Akt independent of ras mutational status. Clin Cancer Res 2010;16:912-23.
30. Andersson MK, Aman P. Proliferation of Ewing sarcoma cell lines is suppressed by the receptor tyrosine kinase inhibitors gefitinib and vandetanib. Cancer Cell Int 2008;8:1.
