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Thursday, April 14, 2016 4:42:18 PM
Remember a long time ago when I said that mesenchymal subtype was more important to overall response than methylation over on SA? Your thought process here reflects why. I had read that DC treatments were seeing better response on mesenchymal and that methylation was not as important except in strengthening this response. We now know that immunogenicity is created by increased production of neo antigens which happens with mesenchymal genotype (original form) and mesenchymal phenotype (caused by mutation from chemo/radiation intervention). Type of response to treatment appears highly correlated to the degree that mesenchymal expression actually occurs in each tumor and creates the critical T-cell targets that Dr. Prins mentioned. The observed measurable immune response potential appears to remain at the 80%-85% level as NWBO has previously reported and some of these would need CIs to improve OS outcome as there would still be a less than ideal biomarker profile and TILs in changed phenotype until, as you say, the crossover helps to upload them and immunosupression is controlled.
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