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Utilizing two discrete murine HCC models, we found that myeloid-specific deletion of Samhd1 promotes HCC progression through increased PD-L1 expression and CXCL1/2-mediated recruitment and activation of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs)

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But having set the bar, Novo failed to clear it in data published Friday

10.1016/0140-6736(90)91812-O