Replies to post #30129 on NorthWest Biotherapeutics Inc (NWBO)

[CaptainObvious]

Ya don't want to be 0 on the Karnosfky scale.

[Rkmatters]

And in this document it shows ID1H highest in early stage brain cancers. In GBM, it makes up 12 percent. Those tend to be secondary cancers (meaning it didn't start as GBM) and those ID1H mutation is again in Proneural and Neural patients only.

http://www.mdpi.com/2072-6694/3/1/1129/pdf

So in the end, why is this significant? Because it shows that the 2014 chart from NIH study of gene subtypes is accurate. And that the gene subtype split for GBM is:

Proneural: 13 percent
Neural: 12 percent
Classical: 26 percent
Mesenchymal: 49 percent

And why is this important? As it shows Linda Liau DCVax did not cherry pick gene group patients in earlier DCVax trials. She took all term responders in her study, but primarily ended up with a big mix of Mesenchymal, and understandable so, as that is the natural gene make up of GBM. So when the second PI/PII was reported, and when 6 patients were still alive and the median of the trial hadn't been reached, DCVax was the reason why.
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Data from the second Phase I clinical trial, which began in November 2002, continues to mature and as of August 8, 2006 the findings appear to be even more striking than the data from the first Phase I trial. For example:

6 out of 10 patients are still alive, with the median survival not yet reached;
5 of these 6 patients continue to be cancer-free, with no recurrence and with the median follow-up time of 37 months;
Survival times in the trial now range up to 44.4 months (and continuing)
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We all know, a few of these Mesenchymal patients are still alive today. Typical with GBM, is on 3-5 % of patients see survival over 5 years.
(Again, the prior results do not mean that the other gene groups are not responding; it only means that because there were more Mesenchymal patients typically in GBM, it was easier to show the results were not related to chance).
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And lastly, because DCVax-L Ph III trial is for 348 patients, chances are a good mix of patients will be Mesenchymal (if we were to assume it only works in one gene subtype) and see similar PFS/OS results. And, because of that GBM gene type split mix, it's very easy for me to see that is why events were not occurring, and that is why at the blind statistician look of data the trial was resized.