Lol, WW, I noted the same thing – hence a bit of overlap in our posts!
The Stanford University School of Medicine released a research paper in March 2016 titled Myc regulates the antitumor response through CD47 and PD-L1.
I see that this research paper has attracted plenty of interest (1,2). Interestingly, Phylogica referenced this paper in its latest Biotech Showcase presentation.
Slide 43, which shows results from studies conducted by theCancer Epigenetics Lab at the Harry Perkins Institute, reads
Increased cell death, decreased proliferation & PDL1 expression in tumours treated with FPP-Omomyc versus FPP, Omomyc or vehicle control
Potential immuno-oncology implications (3)
It makes me wonder, could the above results have been further improved by combining FPP-Omomyc with a PD-L1 inhibitor?
I note the following comments in a Stanford Medicine blog about the above paper.
The work, published today in Science, is the first to directly link the levels of Myc, CD-47 and PD-L1, and may provide new therapeutic avenues for clinicians….
The research suggests that targeting both Myc expression and that of CD47 or PD-L1 might provide a therapeutic synergy that would be more effective than any treatment alone. (4)
In the animal studies conducted at the Harry Perkins Institute, it was demonstrated that an FPP-Omomyc fusion has strong synergy with Cetuximab, an anti-EGFR antibody. That combination was more than three times more effective at killing drug resistant breast cancer cells than either of these agents alone (See Slide 38) (5).
The currently marketed high profile PD-L1 inhibitors are the antibody therapies Keytruda (Merck) and Opdivo (BMS). Might there be potential for increased effectiveness of these therapies by combining them with FPP- iMYC ?
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(20min delay)