Genetic interrogation of STAT6-mediated macrophage polarization to tumorigenesis in a sterile, penetrant, autochthonous cancer model

Macrophage recruitment into tumors is correlated with poor outcomes in cancer, which correlate with STAT6-dependent M2 macrophage polarization and wound healing-type responses. Using penetrant, genetic models of neuroblastoma, we found macrophage recruitment was protective against tumor formation while disabling STAT6-mediated M2 polarization had no effect on tumorigenesis, progression or expression of key immunosuppressive pathways. Thus while macrophages are drivers of cancer in this model, non-classical M2 STAT6-independent pathways are plausible targets for cancer therapy. ALK TH-MYCN NB tumor model in C57BL\6 x 129Sv/J