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Re: marzan post# 230223

Saturday, 06/01/2019 2:15:04 PM

Saturday, June 01, 2019 2:15:04 PM

Post# of 690766
In your experience, have you seen this many patients about 80+ alive out of 331 total this long for about 45+ months since surgery.

It's definitely odd (in a good way) and it's what drew me to this experimental treatment. If we look at OS in the Stupp protocol for the RT+TMZ group, at 3 years there was 16% OS and at 4 years 12%. Using the numbers you gave me, 80/331 would be 24% OS at 3.75 years (45 months). That's possibly double the OS of Stupp. There's a good chance that most of those patients received the intervention, which could be driving that number. Any way you slice it though, that number higher than Stupp.

Is there still a possibility L being as effective as SOC?

Yes, there's always that possibility. As I have said in other posts, any potential confounders measured or unmeasured can influence the outcome.

How comes Checkpoint Inhibitors are approved left and right. They employ the same dendritic cells to attack the tumor once their breaker is turned off, imo. In DcVax the very same dendritic cells are amplified and processed to be more potent with all the tumor proteins impregnated as a vaccine. Which one in your opinion will do a better job?

I can't speak to why they are routinely approved. Checkpoint inhibitors use monoclonal antibodies to block CTLA-4, PD-1, and PD-L1, which are molecules that inhibit immune cell activity. These are able to restore immune function in the tumor environment by various pathways, but usually T-Cell activation. Dendritic cells are antigen presenting cells. They are messengers that tell the T or B cells what to do. They "prime" them, in a sense, on what to target. They have been shown to assist with PD-1 checkpoint inhibitors. Checkpoint inhibitors will turn off the immune inhibition indiscriminately and can cause side effects (causing an upregulation of an immune response, basically like a drug induced autoimmune disorder). A dendritic cell that has been primed with a specific tumor antigen and then presents this to a T cell, the T cell now knows it must go kill that specific tumor. If dendritic cell therapy works, it should work way better. I think at this stage it may have applications in microscopic residual disease. I'm not convinced on gross tumor, yet. Tumors have many many ways of evading treatments, but seem to be more vulnerable when microscopic versus gross.
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