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• W4361951996 abstract "<div>Abstract<p><b>Purpose:</b> <i>KRAS</i> is the most commonly mutated oncogene in human tumors. <i>KRAS</i>-mutant cells may exhibit resistance to the allosteric MEK1/2 inhibitor selumetinib (AZD6244; ARRY-142886) and allosteric AKT inhibitors (such as MK-2206), the combination of which may overcome resistance to both monotherapies.</p><p><b>Experimental Design:</b> We conducted a dose/schedule-finding study evaluating MK-2206 and selumetinib in patients with advanced treatment-refractory solid tumors. Recommended dosing schedules were defined as MK-2206 at 135 mg weekly and selumetinib at 100 mg once daily.</p><p><b>Results:</b> Grade 3 rash was the most common dose-limiting toxicity (DLT); other DLTs included grade 4 lipase increase, grade 3 stomatitis, diarrhea, and fatigue, and grade 3 and grade 2 retinal pigment epithelium detachment. There were no meaningful pharmacokinetic drug–drug interactions. Clinical antitumor activity included RECIST 1.0–confirmed partial responses in non–small cell lung cancer and low-grade ovarian carcinoma.</p><p><b>Conclusion:</b> Responses in <i>KRAS</i>-mutant cancers were generally durable. Clinical cotargeting of MEK and AKT signaling may be an important therapeutic strategy in <i>KRAS</i>-driven human malignancies (Trial NCT number NCT01021748). <i>Clin Cancer Res; 21(4); 739–48. ©2014 AACR</i>.</p></div>" @default.
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• W4361951996 date "2023-03-31" @default.
• W4361951996 modified "2023-10-14" @default.
• W4361951996 title "Data from Antitumor Activity in <i>RAS</i>-Driven Tumors by Blocking AKT and MEK" @default.
• W4361951996 doi "https://doi.org/10.1158/1078-0432.c.6524007.v1" @default.
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