Replies to post #473384 on NorthWest Biotherapeutics Inc (NWBO)

[jon_k84]

Ex was specifically saying when comparing the treatment arm vs the placebo arm that the Placebo had better OS. Not PFS.

I actually reread the presentation to see if I missed something, but there is simply no such slide. Additionally, such a slide would be totally meaningless as everyone in the placebo crossed over to DCVax.

I’m assuming what he did was try to superimpose two graphs on each other… one placebo and one treatment arm… which is a totally ridiculous thing to do. Anyone who’s had any sort of training in scientific research knows you can’t do that without access to the raw data. You would, at a minimum, need to know the specific date when each placebo patient started taking DC Vax, and neither of those graphs show that. And even if you did have that info it’s still a meaningless comparison since everyone crossed over DC Vax within a year. Essentially, he’s making up his own statistics, but such are the antics I’ve come to expect from ex.

This is why we trust doctors and PhDs to interpret the data. Unless Ex wants to post his MD for everyone to see, no one should be taking anything he says seriously.

[Evaluate]

you wrote:

Of course, as pointed out by Dr. Mulholland, many patients in the treatment arm appeared to event (which is what PFS measures) soon after receiving the treatment.

elsewhere I read:

Since the use of concomitant temozolomide has become standard in the initial management of GBM, a number of groups have reported an increased incidence of PsPD, defined as an increase in contrast enhancement postradiation that subsequently stabilizes or improves without a change in tumor treatment

So: is it the temozolomide that causes the PsPD, and not necessarily the DCVax-L treatment causing PsPD?
Or would DCVax-L perhaps cause a higher incidence of PsPD than temozolomide alone.
Thus the treatment cohort would experience a higher number of false progression (PFS-events) compared to the placebo cohort>