1 Wang X, Crowe PJ, Goldstein D, Yang JL. STAT3 inhibition, a novel approach to enhancing targeted therapy in human cancers (Review). Int J Oncol. 41, 1181-1191, https://doi.org/10.3892/ijo.2012.1568 (2012).
2 Zhang HF, Lai R. STAT3 in cancer-friend or foe? Cancers. 6, 1408-1440, https://doi.org/10.3390/cancers6031408 (2014).
3 Yu H, Lee H, Herrmann A, Buettner R, Jove R. Revisiting STAT3 signalling in cancer: New and unexpected biological functions. Nat Rev Cancer. 14, 736-746, https://doi.org/10.1038/nrc3818 (2014).
4 Levy DE, Lee CK. What does Stat3 do? J. Clin Invest. 109, 1143-1148, https://doi.org/10.1172/JCI15650 (2002).
5 Bromberg JF, et al. Stat3 as an oncogene. Cell. 98, 295-303, https://doi.org/10.1016/S0092-8674(00)81959-5 (1999).
6 Yang XO, et al. STAT3 regulates cytokine-mediated generation of inflammatory helper T cells. J Biol Chem. 282, 9358-9363, https://doi.org/10.1074/jbc.C600321200 (2007).
7 Aggarwal BB, et al. Targeting signal-transducer-and-activator-of-transcription-3 for prevention and therapy of cancer. Ann NY Acad Sci. 1091, 151-169, https://doi.org/10.1196/annals.1378.063 (2006).
8 Nishisaka F, et al. Antitumor activity of a novel oral signal transducer and activator of transcription 3 inhibitor YHO-1701. Cancer Sci. 111, 1774-1784, https://doi.org/10.1111/cas.14369 (2020).
9 Tanizaki J, et al. Combined effect of ALK and MEK inhibitors in EML4-ALK-positive non-small-cell lung cancer cells. Br J Cancer. 160, 763-767, https://doi.org/10.1038/bjc.2011.586 (2012).
10 Bayliss R, Choi J, Fennell DA, Fry AM, Richards MW. Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs. Cell Mol Life Sci. 73, 1209-1224, https://doi.org/10.1007/s00018-015-2117-6 (2016).
11 Choi YL, et al. EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors. N Engl J Med. 363, 1734-1739, https://doi.org/10.1056/NEJMoa1007478 (2010).
12 Sasaki T, et al. A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors. Cancer Res. 71, 6051-6060, https://doi.org/10.1158/0008-5472.CAN-11-1340 (2011).
13 Doebele RC, et al. Mechanisms of resistance to crizotinib in patients with ALK gene rearranged non-small cell lung cancer. Clin Cancer Res. 18, 1472-1482, https://doi.org/10.1158/1078-0432.CCR-11-2906 (2012).
14 Katayama R, et al. Mechanisms of acquired crizotinib resistance in ALK-rearranged lung Cancers. Sci Transl Med. 4, 120ra117, https://doi.org/10.1126/scitranslmed.3003316 (2012).
15 Rolfo C, et al. ALK and crizotinib: after the honeymoon…what else? Resistance mechanisms and new therapies to overcome it. Transl Lung Cancer Res. 3, 250-261, https://doi.org/10.3978/j.issn.2218-6751.2014.03.01 (2014).
16 Miyawaki M, et al. Overcoming EGFR Bypass Signal-Induced Acquired Resistance to ALK Tyrosine Kinase Inhibitors in ALK-Translocated Lung Cancer. Mol Cancer Res. 15, 106-114, https://doi.org/10.1158/1541-7786.mcr-16-0211 (2017).
17 Crystal AS, et al. Patient-derived models of acquired resistance can identify effective drug combinations for cancer. Science. 346, 1480-1486, https://doi.org/10.1126/science.1254721 (2014).
18 Aoki Y, Feldman GM, Tosato G. Inhibition of STAT3 signaling induces apoptosis and decreases survivin expression in primary effusion lymphoma. Blood. 101, 1535-1542, https://doi.org/10.1182/blood-2002-07-2130 (2003).
19 Holbeck SL, et al. The National Cancer Institute ALMANAC: A Comprehensive Screening Resource for the Detection of Anticancer Drug Pairs with Enhanced Therapeutic Activity. Cancer Res. 77, 3564-3576, https://doi.org/10.1158/0008-5472.CAN-17-0489 (2017).
20 Sidorov P, Naulaerts S, Ariey-Bonnet J, Pasquier E, Ballester PJ. Predicting synergism of cancer drug combinations using NCI-ALMANAC data. Front Chem. 7, 509, https://doi.org/10.3389/fchem.2019.00509 (2019).
21 Kobayashi S, et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med. 352, 786-792, https://doi.org/10.1056/NEJMoa044238 (2005).
22 Pao W, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med. 2, e73, https://doi.org/10.1371/journal.pmed.0020073 (2005).
23 Sequist LV, et al. Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors. Sci Transl Med. 3, 75ra26, https://doi.org/10.1126/scitranslmed.3002003 (2011).
24 Yu HA, et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers. Clin Cancer Res. 19, 2240-2247, https://doi.org/10.1158/1078-0432.CCR-12-2246 (2013).
25 Remon J, Steuer CE, Ramalingam SS, Felip E. Osimertinib and other third-generation EGFR TKI in EGFR-mutant NSCLC patients. Ann Oncol. 29, i20-i27, https://doi.org/10.1093/annonc/mdx704 (2018).
26 Chaib I, et al. Co-activation of STAT3 and YES-Associated Protein 1 (YAP1) Pathway in EGFR-Mutant NSCLC. J Natl Cancer Inst. 109, djx014, https://doi.org/10.1093/jnci/djx014 (2017).
27 Song L, Rawal B, Nemeth JA, Haura EB. JAK1 Activates STAT3 Activity in Non-Small-Cell Lung Cancer Cells and IL-6 Neutralizing Antibodies Can Suppress JAK1-STAT3 Signaling. Mol Cancer Ther. 10, 481-494, https://doi.org/10.1158/1535-7163.MCT-10-0502 (2011).
28 Rikova K, et al. Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell. 131, 1190-1203, https://doi.org/10.1016/j.cell.2007.11.025 (2007).
29 Koivunen JP, et al. EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancer. Clin Cancer Res. 14, 4275-4283, https://doi.org/10.1158/1078-0432.CCR-08-0168 (2008).
30 Tanimoto A, et al. Receptor ligand-triggered resistance to alectinib and its circumvention by Hsp90 inhibition in EML4-ALK lung cancer cells. Oncotarget. 5, 4920-4928, https://doi.org/10.18632/oncotarget.2055 (2014).
31 Kogita A, et al. Activated MET acts as a salvage signal after treatment with alectinib, a selective ALK inhibitor, in ALK-positive non-small cell lung cancer. Int J Ooncol. 46, 1025-1030, https://doi.org/10.3892/ijo.2014.2797 (2015).
32 Ariyawutyakorn W, Saichaemchan S, Varella-Garcia M. Understanding and Targeting MET Signaling in Solid Tumors - Are We There Yet? J Cancer. 7, 633-649, https://doi.org/10.7150/jca.12663 (2016).
33 Song L, Turkson J, Karras JG, Jove R, Haura EB. Activation of Stat3 by receptor tyrosine kinases and cytokines regulates survival in human non-small cell carcinoma cells. Oncogene. 22, 4150-4165, https://doi.org/10.1038/sj.onc.1206479 (2003).
34 Mehta R, et al. Deguelin Action Involves c-Met and EGFR Signaling Pathways in Triple Negative Breast Cancer Cells. PLoS One. 8, e65113, https://doi.org/10.1371/journal.pone.0065113 (2013).
35 Mahmoudian-Sani MR, Alghasi A, Saeedi-Boroujeni A, Jalali A, Jamshidi M, Khodadadi A. Survivin as a diagnostic and therapeutic marker for thyroid cancer. Pathology Res Pract. 215, 619-625, https://doi.org/10.1016/j.prp.2019.01.025 (2019).
36 Veiga GLD, et al. The role of Survivin as a biomarker and potential prognostic factor for breast cancer. Rev Assoc Med Bras. 65, 893-901, https://doi.org/10.1590/1806-92220.127.116.113 (1992).
37 Namekawa T, Ikeda K, Horie-Inoue K, Inoue S. Application of Prostate Cancer Models for Preclinical Study: Advantages and Limitations of Cell Lines, Patient-Derived Xenografts, and Three-Dimensional Culture of Patient-Derived Cells. Cells. 8, 74, https://doi.org/10.3390/cells8010074 (2019).
38 Kopetz S, Lemos R, Powis G. The promise of patient-derived xenografts: The best laid plans of mice and men. Clin Cancer Res. 18, 5160-5162, https://doi.org/10.1158/1078-0432.CCR-12-2408 (2012).
39 Daniel VC, et al. A primary xenograft model of small-cell lung cancer reveals irreversible changes in gene expression imposed by culture in vitro. Cancer Res. 69, 3364-3373, https://doi.org/10.1158/0008-5472.CAN-08-4210 (2009).
40 Haibara H, et al. YPC-21661 and YPC-22026, novel small molecules, inhibit ZNF143 activity in vitro and in vivo. Cancer Sci. 108, 1042-1048, https://doi.org/10.1111/cas.13199 (2017).
41 Chou TC. Drug combination studies and their synergy quantification using the Chou-Talalay method. Cancer Res. 15, 440-446, https://doi.org/10.1158/0008-5472.CAN-09-1947 (2010).
42 Taniguchi K, Nishiura H, Ota Y, Yamamoto T. Roles of the Ribosomal Protein S19 Dimer and Chemically Induced Apoptotic Cells as a Tumor Vaccine in Syngeneic Mouse Transplantation Models. J Immunother. 34, 16-27, https://doi.org/10.1097/CJI.0b013e3181fb03ed (2011).
43 Taniguchi K, Nishiura H, Yamamoto T. Requirement of the Acquired Immune System in Successful Cancer Chemotherapy with cis-Diamminedichloroplatinum (II) in a Syngeneic Mouse Tumor Transplantation Model. J Immunother. 34, 480-489, https://doi.org/10.1097/CJI.0b013e31821e7662 (2011).