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10.1172/JCI80006

http://scihub22266oqcxt.onion/10.1172/JCI80006
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suck abstract from ncbi


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pmid26325033
      J+Clin+Invest 2015 ; 125 (9 ): 3365-76
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  • Tumor-induced myeloid deviation: when myeloid-derived suppressor cells meet tumor-associated macrophages #MMPMID26325033
  • Ugel S ; De Sanctis F ; Mandruzzato S ; Bronte V
  • J Clin Invest 2015[Sep]; 125 (9 ): 3365-76 PMID26325033 show ga
  • The generation of an inflammatory environment is favorable and often decisive for the growth of both primary tumors and metastases. Tumor cells either express membrane molecules or release tumor-derived soluble factors able to alter myelopoiesis. Tumor-reprogrammed myeloid cells not only create a tolerogenic environment by blocking T cell functions and proliferation, but also directly drive tumor growth by promoting cancer stemness, angiogenesis, stroma deposition, epithelial-to-mesenchymal transition, and metastasis formation. In this Review, we discuss the interplay between immunosuppressive and protumoral myeloid cells and detail their immune-regulatory mechanisms, the molecular pathways involved in their differentiation, as well as their potential role as prognostic and diagnostic biomarkers and prospective targets for innovative approaches to treat tumor-bearing hosts.
  • |*Immune Tolerance [MESH]
  • |Animals [MESH]
  • |Biomarkers, Tumor/*immunology [MESH]
  • |Cell Differentiation/*immunology [MESH]
  • |Epithelial-Mesenchymal Transition/*immunology [MESH]
  • |Humans [MESH]
  • |Macrophages/*immunology/pathology [MESH]
  • |Neoplasm Metastasis [MESH]
  • |Neoplasms/diagnosis/*immunology/pathology [MESH]
  • |Prognosis [MESH]


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