Saturday, July 23, 2016 4:27:47 PM
Going after residual cells that can travel is not something TMZ or radiation does well.
Eventually even the CUA survivors curve will make regulators question what is going on under the hood. You know that I argued that a good portion of those "indeterminate" survivor patients are psPD. I still believe that to be the case. But even psPD GBM patients have an expected lifespan. If as a curve the indeterminate moves passed expected survival of psPD then eventually all these long tail survival can't just be termed chance.
I don't know if you saw my last post to Exwannabe, in it I posted 4 patterns of responses that are being seen with immunotherapy. I like them all, but I particularly think #3 is not talked about often enough:
3) case with patterns where the immune system is in some form of equilibrium state with the tumor; and it leads to prolonged stabilization of disease. That may over time lead to a conventional response but it may take time to a year or more for that to happen.
This "equilibrium" immune state that an immunotherapy can have with the tumor can be used to show a delay in PFS efficacy can correlated to a prolonged effect in OS. There may be patients who walk around with no disease or residual tumor load (cancer that is fighting back in order to stick around in the patient) and DCVax-L injections could helping to keep the disease dormant or in check, where it's evident; if this is happening clinical investigators will be able to measure "tumor" changes (or not) and record the phenomenon. That will be important distinction for GTR and Partial Resection patients. If the immunotherapy is able to stop spread of disease, and it is then a matter of keeping the whatever disease remains in check, stable but not growing, it could lead to overwhelming OS efficacy. Chemotherapy has no immunotherapy effect. It either shrinks the tumor or it doesn't. But immunotherapy can shrink a tumor; it can grow a tumor, then shrink it; keep the size of the tumor the same, then possible shrink or grow it; or it can lead to T cell accumulation to new lesions. This #3 efficacy "keep it in check" pattern can be the curve ball this study sees. How slow and stable is the GBM disease in the patients? Are they seeing many cases where patients have GBM residual tumor load but the size has not grown to be considered progression? These are things we don't know. But I expect they are seeing stable disease in this GBM study and in other diverse cancers.
My hope is that a number of Direct patients went onto try other immunotherapies and are seeing a response. And that all former patients will be allowed to go on a CI to see if that can enhance their response if they are not on one already. If so, then the patients who only see a stable disease response can possible go onto to see a conventional response.
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