That may be the case, but these kinds of biomarkers are far, far from ready for primetime for use in patient selection. Proteomics and relentless pursuit notwithstanding, we have not gotten any evidence of a predictive biomarker that is remotely ready.
And the level of evidence to justify a predictive biomarker is pretty high. Something like HER2 positivity, microsatellite instability, RET fusion, BRAF mutation, and NTRK fusions have shown pretty conclusively (some moreso than others) that a targeted/immunologic therapy that exploits those biomarkers will give a high chance of at least an objective response, and in the case of several of these biomarkers, that treatment with the agent will improve overall survival.
But only in the patients who have the marker, and that's the reason that those I listed above have tissue-agnostic (or nearly tissue agnostic in the case of dabrafenib-trametinib in colorectal, but a bit of a moot point since the BREAKWATER study readout earlier this year).
Importantly, these biomarkers we're discussing would need to inform on which patients should NOT receive therapy. For example, pembrolizumab shouldn't just be tried for any patient. It either has its bevy of specific labeled indications, or it's MSI-H tissue agnostic (TMB, too, but TMB is more controversial).
I don't think such a thing exists for DCVax, and we're not likely to find it soon. If NWBO had a biomarker that could tell which of those patients were more likely NOT to benefit, it would be a pretty easy path to global approval. As it stands, the best information we have is that the phase 3 trial showed a statistically significant OS improvement for DCVax-L added to standard of care compared with control arms from contemporary studies.
What comes to mind quickest is the role of ctDNA, especially in adjuvant therapy for colon cancer. It has massive prognostic value (ie, if after surgery you have detectable ctDNA, you are nearly guarantee to have disease recurrence; if eliminated, you're very likely to be cured, possibly without undergoing chemotherapy after surgery).
But they can't nail down the right situation to make that predictive, even with the strong evidence we have in our hands. The oncologists I work with have these debates all the time in our programs, whether ctDNA should be used to "guide" therapy (ie, if a patient is positive for ctDNA after surgery or chemotherapy, should you chase elimination of it?). The answer isn't there, and as a result it still has not been added to guidelines, even after many promising early trials and at least one randomized study (DYNAMIC) that really appeared to support "ctDNA-guided" decision making for adjuvant chemotherapy.
A long way of supporting the idea that, translational research notwithstanding, and there has been and will be a lot, it's a lot harder to move that to clinical decision making, unless it ends up being a more binary biomarker like EGFR mutation, which can really give you a clear idea of what to do for the patient.
I suppose you could read that as good or bad for this current story. If it's approved for GBM, there's no way that it would be restricted to a biomarker-positive population, because there hasn't been one identified. But on the other hand, without such an exclusionary biomarker, the chance for a tissue-agnostic approval is vanishingly small, administrative labeling within this particular spreadsheet or not.
On a separate note, when did this document become available to the public? The listing was changed April 1, but if it came out in public later, do we think that could be the impetus for the run-up in share price? It would certainly seem like something worthy of building excitement.
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