I'll be glad to talk the science. Of course any such posts by me will be met with nothing but personal attacks and no ability to counter the actual content.
Here goes.
What we know about the science is that it is one on hundreds of attempts to produce a DC Vaccine. And many processes have been very similar. What NWBO has always stated as their claim to being special is the ability to manufacturer in a single run.
Certainly there are various modest tweaks in all these that can make a difference, but nobody here knows what exactly is different in the science in that respect. And I doubt even anybody at NWBO (or UCLA) knows. The truth is even experts simply do not know the science well enough to say why a couple hours difference in maturation time is improving OS. If they did, they would not be trialing all these combinations.
Hand waving arguments that it attacks all antigens, that it is God's method, that it works for everything are worthless. That is not science, that is pumping.
So we get to what is left, and that is the trial data,
The design of the trial was that from post surgery to progression 232 would receive DCVax-L and 99 placebo. After progression they would all do whatever (they blindly chose to stay on -L or not, could add any approved treatment, and if not staying on -L could add any experimental treatment). Not an unusual design.
The idea was that even though after progression the OS would be confounded, -L should still show a separation based on the pre-progression treatment. And that failed. The 232 did not live any longer than the 99. And that is a huge issue no matter how much longs want to ignore it.
Oh, longs will argue that it is the crossover effect that cause the 99 to do as well (or even trend better) than the 232. But that is just an unproven assertion. Cannot be proven from within the trial data.
So after seeing the trial as designed failed NWBO changed the plan to compare the 232 to ECAs. But this is tricky, it requires careful planning to insure comparable ECAs exist. That is why the FDA guidances that are frequently cited by longs note how important it is to design the trial in advance properly. It is why the FDA wants to see patient level data on the ECAs.
So now we have a trial that failed the predefined OS badly, and a poorly implemented ad-hoc (yes, it was) attempt to salvage it,
The longs will counter it with "but they really did live longer". The problem is that if one selects patients carefully they will as long as they did in the -L trial. The -L trial selected 331 of about 1500 patients. But it is actually worse than that as many patients would not have applied as they were clearly not suitable for the "intent for near total resection:" criterion.
But dig deeper on that. In the trial patients with near total resections[ntr] on -L did no better than those on placebo. Think about that. You need "intent" for ntr to be in the trial, yet if you have it you do no benefit. The entire benefit was in comparing -L w/o ntr to ECAs w/o ntr. But that is hugely apples to oranges as the ECA had biopsies and patients for who only partials were planned.
In short, there is no reason to think that if patients receive near total resection, are able to get off steroids and show no signs of progression in the first few months they do not live a relatively long time.
Taking a step back, it is not about proving what I am saying, it is about the simple fact that the trial did not prove otherwise.
Waiting for all the "science" replies.
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