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@ARTICLE{Yang:294754,
      author       = {C. Yang$^*$ and H. Geng and X. Yang and S. Ji and Z. Liu
                      and H. Feng and Q. Li and T. Zhang and S. Zhang and X. Ma
                      and C. Zhu and N. Xu and Y. Xia and Y. Li and H. Wang and C.
                      Yu and S. Du$^*$ and B. Miao$^*$ and L. Xu and H. Wang and
                      Y. Cao and B. Li and L. Zhu and X. Tang and H. Zhang and C.
                      Zhu and Z. Huang and C. Leng and H. Hu and X. Chen and S.
                      Yuan and G. Jin and R. Bernards and C. Sun$^*$ and Q. Zheng
                      and W. Qin and Q. Gao and C. Wang},
      title        = {{T}argeting the immune privilege of tumor-initiating cells
                      to enhance cancer immunotherapy.},
      journal      = {Cancer cell},
      volume       = {42},
      number       = {12},
      issn         = {1535-6108},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-02469},
      pages        = {2064-2081.e19},
      year         = {2024},
      note         = {#EA:D250# /2024 Dec 9;42(12):2064-2081.e19},
      abstract     = {Tumor-initiating cells (TICs) possess the ability to evade
                      anti-tumor immunity, potentially explaining many failures of
                      cancer immunotherapy. Here, we identify CD49f as a prominent
                      marker for discerning TICs in hepatocellular carcinoma
                      (HCC), outperforming other commonly used TIC markers.
                      CD49f-high TICs specifically recruit tumor-promoting
                      neutrophils via the CXCL2-CXCR2 axis and create an
                      immunosuppressive milieu in the tumor microenvironment
                      (TME). Reciprocally, the neutrophils reprogram nearby tumor
                      cells toward a TIC phenotype via secreting CCL4. These cells
                      can evade CD8+ T cell-mediated killing through
                      CCL4/STAT3-induced and CD49f-stabilized CD155 expression.
                      Notably, while aberrant CD155 expression contributes to
                      immune suppression, it also represents a TIC-specific
                      vulnerability. We demonstrate that either CD155 deletion or
                      antibody blockade significantly enhances sensitivity to
                      anti-PD-1 therapy in preclinical HCC models. Our findings
                      reveal a new mechanism of tumor immune evasion and provide a
                      rationale for combining CD155 blockade with anti-PD-1/PD-L1
                      therapy in HCC.},
      keywords     = {CITE-seq (Other) / hepatocellular carcinoma (Other) /
                      immunotherapy (Other) / tumor-associated neutrophils (Other)
                      / tumor-initiating cells (Other)},
      cin          = {D250},
      ddc          = {610},
      cid          = {I:(DE-He78)D250-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39515328},
      doi          = {10.1016/j.ccell.2024.10.008},
      url          = {https://inrepo02.dkfz.de/record/294754},
}