From what I can tell, the addition will be a little less than the exclusion. Someone can correct me. I’ll leave it at that.
I think UCLA did some small DC treatment studies on those being added. I’ll give my parking spot to anyone that can confirm that. A very very promising connection, if I’m right.
It may not work as well on pronumeral initially but then there is this (below). So maybe we can give proneural patients, dare I say it (Avastin), to promote a mesenchymal transition and then DCVAX. Again note, Mesenchymal is associated with enhanced aggressiveness and poorer prognosis, but seems to be great for DCVAX. I wonder if this is similar to how checkpoints do better with more mutational burden.
"It is now established that an epithelial-mesenchymal-like transition (EMT), termed as proneural-mesenchymal transition (PMT), exists in GBM [16, 35, 37]. Analysis performed on paired GBM specimens prior to radiotherapy and at the time of recurrence suggested that there is a shift of the glioma cells from the proneural to the mesenchymal phenotype [16]. In addition, transcription factors that play important role in EMT, such as twist family BHLH transcription factor-1 (TWIST-1), zinc finger E-box binding homeobox-1 (ZEB-1)/ZEB-2, and snail family transcriptional repressor-1 (SNAIL-1)/SNAIL-2, were found to be altered in GBM [38, 39] as the proneural cells undergo transformation to mesenchymal subtype. Downregulation of proneural-specific markers and upregulation of mesenchymal-specific markers were also observed in irradiated proneural glioma cells [35]. Furthermore, elevated levels of mesenchymal markers expression were observed in mouse xenograft model treated with bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF) [37]. The shift from proneural to mesenchymal phenotype may account for the enhanced aggressiveness observed in patients with recurrent glioma that have acquired resistance to bevacizumab [37]"
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