What we did is we looked at the results of the phase 3 trial using selinexor as a maintenance treatment in cases of advanced and relapsed endometrial cancer after treatment with chemotherapy with paclitaxel and carboplatin. And in a randomized, placebo-controlled trial, we have seen huge differences in patients with P53 wild-type, which is a huge cohort in women with endometrial cancer with a significant and clinically relevant impact on progression-free survival and overall survival...
What we did is we looked at the results of the phase 3 trial using selinexor as a maintenance treatment in cases of advanced and relapsed endometrial cancer after treatment with chemotherapy with paclitaxel and carboplatin. And in a randomized, placebo-controlled trial, we have seen huge differences in patients with P53 wild-type, which is a huge cohort in women with endometrial cancer with a significant and clinically relevant impact on progression-free survival and overall survival. And then we did now the subgroup analyses to look if we have tumors with P53 wild-type but in relationship to the microsatellite instability status to look if this effect is consistent. And even in both groups, in the proficient group and in the deficient group, we can see the significant impact of giving selinexor as a maintenance treatment. So this is across even the subtypes of subtypes. And we are, I think, learning that endometrial cancer patients have maybe much more different subtypes based on our molecular signature. But in case of this drug, what we can see, it is independent from the microsatellite instability status. What is even the question, if it’s maybe better to treat with a checkpoint inhibitor, but we can say it’s independent.
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