CSIG-39. PROSTAGLANDIN-SCULPTING; REPRODUCTIVE DRIVERS OF THE GBM TUMOR IMMUNE LANDSCAPE

Abstract Introduction We have reported that GBM utilize sex-steroids and reproduction-specific proteins to hijack the granting of immune-privilege male/partner-specific antigens/epitopes. extended upon this foundation examine other examples immunosuppressive tissue-mimicry mechanisms deploy. The generation prostaglandins D2, E2 F2 reproductive are used by tumors activate discrete immune-cell types drive vascularization growth. METHODS Three GBM-transcriptome databases were mined analyzed utilizing pathway, stratification, correlation survival analysis. RESULTS PGD2 PGF2 synthesis is driven C3AR1 microglial signaling, in response complement C3a activation expression C3 CFB. expressed hypoxic normoxic ones. drives hematopoietic stem cell angiogenic via TPBG/CXCL12/CXCR4. This primary pathway promoting early placental vascular development/repair mucosal tissues. Microglial synthesized CCL5/CCR5 axis, a central cyclic uterine tissues wound healing, VEGFA. Generation CCL5 also recruits CCR5-positive monocytes, which then into M2-TAM phenotype. myeloid cells MDSCs. SOX9 masculinization embryonic gonads. correlates with seminal heat shock protein expression. These HSPs associated neutrophil PGE2 tumors, mirroring their role semenized female tract, where they support aid EGFR CONCLUSIONS ability modulate anti-tumor lethality. discrete, cell-specific revealed will allow personalized medicine using off-the-shelf drug therapy.