exwannabe,
Recurrent patients crossed over to L did much better than those that either did not crossover in the trial or those external rGBM comparators. What you fail to mention consistently is that rGBM vs rGBM in any setting has pretty standard survival rates which is why there is no SOC for rGBM and no advance in treatment for so long. So rGBM crossover survival from SOC/placebo original patients added to the OS rate for SOC/placebo original patients because the original measures were inadequate to measure actual treatment effect. If there was no treatment effect the rGBM patients from any source would all have fallen into the historical range of survival and this trial proves that was not the case hence the crossover was to an active treatment, which by the way, is known to be more active in mesenchymal signature patients which is the phenotype signature for ~85% of all rGBM patients and only about a 40-50% rate in primary GBM. This discrepancy alone easily accounts for SOC/placebo crossover patients responding at a higher rate than treatment arm crossover which was much more likely to be a crossover to placebo even though longest living survivors were advantaged by early treatment vs later treatment. That’s the bird’s eye view. Best wishes.
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