Martini, G; Cardone, C; Vitiello, PP; Belli, V; Napolitano, S; Troiani, T; Ciardiello, D; Della Corte, CM; Morgillo, F; Matrone, N; Sforza, V; Papaccio, G; Desiderio, V; Paul, MC; Moreno-Viedma, V; Normanno, N; Rachiglio, AM; Tirino, V; Maiello, E; Latiano, TP; Rizzi, D; Signoriello, G; Sibilia, M; Ciardiello, F; Martinelli, E in [Martini, Giulia; Cardone, Claudia; Vitiello, Pietro Paolo; Belli, Valentina; Napolitano, Stefania; Troiani, Teresa; Ciardiello, Davide; Della Corte, Carminia Maria; Morgillo, Floriana; Matrone, Nunzia; Ciardiello, Fortunato; Martinelli, Erika] Univ Campania L Vanvitelli, Med Oncol, Dept Precis Med, Via Pansini 5, I-80131 Naples, Italy; [Sforza, Vincenzo] Fdn Pascale, IRCCS, Ist Nazl Tumori, Dept Clin Expt Thorac Oncol, Naples, Italy; [Papaccio, Gianpaolo; Desiderio, Vincenzo; Tirino, Virginia] Univ Campania Luigi Vanvitelli Napoli, Dept Expt Med, Naples, Italy; [Paul, Mariel C.; Moreno-Viedma, Veronica; Sibilia, Maria] Med Univ Vienna, Comprehens Canc Ctr, Dept Med 1, Inst Canc Res, Borschkegasse 8a, Vienna, Austria; [Normanno, Nicola; Rachiglio, Anna Maria] Fdn Pascale, IRCCS, Ist Nazl Tumori, Cell Biol & Biotherapy Unit, Naples, Italy; [Maiello, Evaristo; Latiano, Tiziana Pia; Rizzi, Daniele] Hosp Casa Sollievo Della Sofferenza San Giovanni, Med Oncol, San Giovanni Rotondo, Italy; [Signoriello, Giuseppe] Univ Campania L Vanvitelli, Biostat, Dipartimento Salute Mentale & Fis & Med Prevent, Naples, Italy published EPHA2 Is a Predictive Biomarker of Resistance and a Potential Therapeutic Target for Improving Antiepidermal Growth Factor Receptor Therapy in Colorectal Cancer in 2019.0, Cited 24.0. SDS of cas: 64-10-8. The Name is 1-Phenylurea. Through research, I have a further understanding and discovery of 64-10-8.
The EPHA2 tyrosine kinase receptor is implicated in tumor progression and targeted therapies resistance. We evaluated EPHA2 as a potential resistance marker to the antiepidermal growth factor receptor (EGFR) monoclonal antibody cetuximab in colorectal cancer. We studied activation of EPHA2 in a panel of human colorectal cancer cell lines sensitive or resistant to anti-EGFR drugs. The in vitro and in vivo effects of ALW-II-41-27 (an EPHA2 inhibitor) and/or cetuximab treatment were tested. Fonnalin-fixed paraffin-embedded tumor specimens from 82 RAS wild-type (WV) metastatic colorectal cancer patients treated with FOLFIRI + cetuximab as first-line therapy in the CAPRI-COIM trial were assessed for EPHA2 expression by immunohistochemistry and correlated with treatment efficacy. EPHA2 was differentially activated in colorectal cancer cell lines. Combined treatment with ALW-II-41-27 plus cetuximab reverted primary and acquired resistance to cetuximab, causing cell growth inhibition, inducing apoptosis and cell-cycle G1-G2 arrest. In tumor xenograft models, upon progression to cetuximab, ALW-II-41-27 addition significantly inhibited tumor growth. EPHA2 protein expression was detected in 55 of 82 tumor samples, frequently expressed in less-differentiated and left-sided tumors. High levels of EPHA2 significantly correlated with worse progression-free survival [8.6 months; confidence interval (CI) 95%, 6.4-10.8; vs. 12.3 months; CI 95%, 10.4-14,2; P = 0.03] and with increased progression rate (29% vs. 9%, P = 0.02). A specific EPHA2 inhibitor reverts in vitro and in vivo primary and acquired resistance to anti-ECFR therapy. EPHA2 levels are significantly associated with worse outcome in patients treated with FOLFIRI + cetuximab. These results highlight EPHA2 as a potential therapeutic target in metastatic colorectal cancer.
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