Probably yes. Virtually all primary or de novo GBMs are wild-type.
Mutated IDH almost always signifies a secondary glioma, whether or not it was recognised as a secondary glioma at the time of initial 'GBM' diagnosis.
And mutated IDH goes with younger age, better prognosis, and a pro-neural signature. But we are only talking about roughly 5% of the GBM population (the 5% that will no longer be called GBM).
Not saying it ever happened, but up until now in GBM trials, there was scope to stick a few more secondary GBMs in your treatment arm compared to your control arm, to give yourself a bit of a fair wind....
Understandably, researchers and regulators want to better categorise the heterogeneous nature of high-grade gliomas to identify which treatments are most likely to be effective in the case of each individual.
And maybe that is why regulators asked for an analysis of the L trial population to identify IDH mutation status and stratify results accordingly. This would enable a stratified comparison with the control arms of those other comparator trials. IDH wild type v IDH wildtype, and IDH mutation v IDH mutation.
Though I doubt those other comparator trials actually ever did comprehensive testing for IDH mutation status.
But an informative comparison can be made between outcomes based on mutation status just within the L trial.
Of course this is where DCVax-L aces it. Because each patient's treatment with L, is based on the unique transcriptional and molecular characteristics of that patient's tumor. And that includes intra-tumoral heterogeneity. And is therefore guaranteed to be a perfect match (especially when used as soon after resection as possible).
I can foresee that L may prove more effective with unmeth patients if TMZ is dispensed with (because it doesn't work for them), and the L injections are started straight away after recovery from surgery (possibly concurrent with some targeted RT).
But that is a side-issue.
L, being completely autologous (tailored to the individual's tumor, and using the individual's primed DC's to do the antigen-presenting) will always be superior (everything else being equal), to allogeneic approaches using synthetic or donor-derived peptides that only target a limited number of an individual's tumor characteristics.
In short, the WHO re-classifications do not make a lot of difference in the case of our trial. L remains the best treatment prospect for the 95% wild-type, precisely because it is fully personalised, and it will probably be best for the 5% mutated IDH as well.
And there is no reason why regulators shouldn't see it this way.
Additionally, L will almost certainly be the most effective option by far, for rGBM patients who weren't able to receive L at the time of initial diagnosis. (Kristyn's Dad is only here because of L.)
What LP told us all those years ago about the importance of a fully personalised approach, remains as true now as it was then.
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