2023
DOI: 10.1016/j.ejca.2023.02.004
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Corrigendum to “Preclinical evaluation of drug combinations identifies co-inhibition of Bcl-2/XL/W and MDM2 as a potential therapy in uveal melanoma” [Eur J Cancer 126 (2020) 93–103]

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“…Additionally, while explaining the role of FAK in signaling pathways and tumor development, we found promising therapeutic targets that can be synergistically combined with FAK. Specifically, significant synergies were noted when FAK inhibitors were combined with mTOR inhibitors (Shi et al, 2016;Cuellar-Vite et al, 2022), RAF/ MEK inhibitors (Capelletto et al, 2022;Gu et al, 2022;Tarin et al, 2023), CDK4/6 inhibitors (Murphy et al, 2022;Peng et al, 2023), MAPK inhibitors (Peng et al, 2023), and VEGF inhibitors such as bevacizumab (Zheng et al, 2023). Furthermore, we observed an upregulation of FAK in specific tumor types with gene mutations or aberrant protein expression, such as BRAF/KRAS mutations, CDH1 deletions, EGFR or HER2 overexpression, and mediated drug resistance processes (Tong et al, 2019;Yuen et al, 2021;Yu et al, 2022;Castro-Guijarro et al, 2023).…”
Section: Summary and Prospectmentioning
confidence: 70%
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“…Additionally, while explaining the role of FAK in signaling pathways and tumor development, we found promising therapeutic targets that can be synergistically combined with FAK. Specifically, significant synergies were noted when FAK inhibitors were combined with mTOR inhibitors (Shi et al, 2016;Cuellar-Vite et al, 2022), RAF/ MEK inhibitors (Capelletto et al, 2022;Gu et al, 2022;Tarin et al, 2023), CDK4/6 inhibitors (Murphy et al, 2022;Peng et al, 2023), MAPK inhibitors (Peng et al, 2023), and VEGF inhibitors such as bevacizumab (Zheng et al, 2023). Furthermore, we observed an upregulation of FAK in specific tumor types with gene mutations or aberrant protein expression, such as BRAF/KRAS mutations, CDH1 deletions, EGFR or HER2 overexpression, and mediated drug resistance processes (Tong et al, 2019;Yuen et al, 2021;Yu et al, 2022;Castro-Guijarro et al, 2023).…”
Section: Summary and Prospectmentioning
confidence: 70%
“…Therefore, the compensatory activation of FAKrelated pathways, such as FAK/SRC and FAK/YAP, is a crucial pathway contributing to the ineffectiveness of single targeted therapies for RAS, RAF, or MEK in KRAS mutant tumors. Combining FAK inhibition therapy can potentially restore the sensitivity of drug-resistant cells to MEK or KRAS inhibitors, improving their anti-tumor effect (Gu et al, 2022;Tarin et al, 2023). Based on these preclinical research findings, a phase II clinical trial (NCT04620330) is currently underway (Capelletto et al, 2022) to investigate the true efficacy of the combination therapy of FAK inhibitor defactinib and the RAF/MEK inhibitor VS-6766 for KRASmutant NSCLC.…”
Section: Ras/raf/mek/erk Signaling Pathwaymentioning
confidence: 99%