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Low-grade slurry ovarian cancer (LGSOC) is less sensitive to chemotherapy.
30%-60% of LGSOC has genetic mutations that affect mapK pathfages, most commonly KRAS/BRAF.
binimetinib is a new MEK1/2 inhibitor that has been shown to be anti-tumor active in a variety of cancers.
there is no data on the drug's use in LGSOC.
conducted a randomized trial with Monk et al. to assess the efficacy and safety of nitinib for LGSOC.
the trial recruited relapsed, detectable LGSOC patients who had underwent 1-3 rounds of chemotherapy and were randomly assigned to the binitinib group (45 mg, 2/day) or the doctor-determined chemotherapy (PCC) group at 2:1.
end point is progress-free survival (PFS).
secondary endpoints are total survival (OS), overall mitigation rate (ORR), mitigation duration (DOR), clinical benefit ratio, biomarkers, and safety.
303 patients as of mid-term analysis on January 20, 2016.
PFS in the
-Benitez and PCC groups was 9.1 months and 10.6 months (HR 1.21; 95% CI 0.79-1.86), respectively, and the study ended early after 341 patients were recruited, based on pre-defined invalid boundaries.
two groups have similar secondary endpoints: ORR 16% vs 13%, Middle DOR 8.1 Months vs 6.7 Months, Middle OS 25.3 Months vs 20.8 Months.
safety results were consistent with the known safety of pythonic acid, and the most common level 3 adverse reaction was an increase in blood creatic acid kinase levels (26%).
post-mortem analysis showed that kraS mutations may affect patients' sensitivity to nitini.
conclusion: Although MEK inhibitors for low-grade slurry ovarian cancer research did not reach their primary endpoint, binitinib also showed anti-tumor activity against LGSOC.
, chemotherapy was more resedative than expected, and patients with KRAS mutations or predictable patients were more sensitive to nitini.
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