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A randomized study (MILO/ENGOT-ov11) reported by Monk and others at the University of Arizona School of Medicine showed that although the MEK inhibitor Binimetinib in the low-grade slurry ovarian cancer (LGSOC) study showed anti-tumor activity in the end-of-efficacy assessment, kraS mutations predicted reactions to Binimetinib.
(J Clin Oncol. doi:10.1200/JCO.20.01164) in the past, LGSOC's response to chemotherapy was low.
most common changes affecting mapK pathways are KRAS/BRAF, which accounts for 30% to 60% of LGSOC.
the purpose of this study is to evaluate in LGSOC an effective MEK1/2 inhibitor, Binimetinib, which is active in a variety of tumors.
patients were randomly grouped at 2.1 and received Binimetinib (45 mg bid) and chemotherapy (PCC) of their doctor's choice, respectively.
: There is ≥ 1 type of platinum-containing chemotherapy, but there is a measurable recurrence of LGSOC after no more than 3 lines of chemotherapy.
end point is the progress-free lifetime (PFS) assessed by BICR.
the in-period analysis (January 20, 2016), a total of 303 patients were random.
PFS was 9.1 months in the Binimetinib group evaluated by BICR, and 10.6 months in the PCC group (HR=1.21,95% CI 0.79-1.86);
two groups had similar secondary efficacy endpoints: ORR of 16% (CR/PR, 32 cases) vs. 13% (13 cases), the medium DOR of 8.1 months vs. 6.7 months, and the middle OS of binimetinib and PCC groups of 25.3 months and 20.8 months, respectively.
results were consistent with known Binimetinib safety, and the most common≥ level 3 adverse event was elevated blood creatinase levels (26%).
analysis suggests that there may be a link between kraS mutations and reactions to Binimetinib.
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