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@ARTICLE{Nadella:141138,
      author       = {V. Nadella and S. Singh and A. Jain and M. Jain and K. M.
                      Vasquez and A. Sharma and P. Tanwar and G. K. Rath and H.
                      Prakash$^*$},
      title        = {{L}ow dose radiation primed i{NOS} + {M}1macrophages
                      modulate angiogenic programming of tumor derived
                      endothelium.},
      journal      = {Molecular carcinogenesis},
      volume       = {57},
      number       = {11},
      issn         = {0899-1987},
      address      = {New York, NY},
      publisher    = {Wiley Interscience},
      reportid     = {DKFZ-2018-01669},
      pages        = {1664 - 1671},
      year         = {2018},
      abstract     = {Solid tumors are covered by stroma, which is hypoxic in
                      nature and composed of various non-malignant components such
                      as endothelial cells, fibroblasts, and pericytes that
                      support tumor growth. Tumor stroma represents a mechanical
                      barrier for tumor infiltration of CD8+ effector T cells in
                      particular. In this context, our previous studies have
                      demonstrated the therapeutic impact of Low-Dose Radiation
                      (LDR)-primed and M1-retuned (iNOS+) peritumoral macrophages
                      that produce inducible nitric oxide, have immunological
                      roles on tumor infiltration of effector T cells,
                      cancer-related inflammation, and subsequent tumor immune
                      rejection in a mouse model of pancreatic cancer. These
                      findings suggested a possible modification of tumor
                      endothelium by LDR-primed macrophages. In line with these
                      observations, here we demonstrate the influence of LDR in
                      down-modulating HIF-1 in irradiated tumors in the course of
                      polarization of irradiated tumor-associated macrophages
                      toward an M1 phenotype. Furthermore, we demonstrate that M1
                      macrophages which are primed by LDR can directly influence
                      angiogenic responses in eNOS+ endothelial cells which
                      produce nitric oxide having both vascular and physiological
                      roles. Furthermore, we demonstrate that naïve macrophages,
                      upon differentiating to an M1 phenotype either by Th1
                      stimuli or LDR, potentially modify
                      sphingosine-1-phosphate/VEGF-induced angiogenic signaling in
                      tumor-derived endothelial cells with tumorigenic potential,
                      thus indicating the significance of iNOS+ macrophages in
                      modulating signaling in eNOS+ tumor-derived endothelium. Our
                      study suggests that iNOS+ macrophages can activate tumor
                      endothelium which may contribute to cancer-directed
                      immunotherapy in particular.},
      cin          = {D015},
      ddc          = {610},
      cid          = {I:(DE-He78)D015-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30035346},
      doi          = {10.1002/mc.22879},
      url          = {https://inrepo02.dkfz.de/record/141138},
}