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@ARTICLE{Haist:309606,
      author       = {M. Haist and M.-A. Baertsch$^*$ and N. E. Reticker-Flynn
                      and G. Lu and T. N. Kempchen$^*$ and P. Chu and G. Vazquez
                      and H. Chen and J. B. Sunwoo$^*$ and W. Zhang and E.
                      Laseinde and B. Adami and S. Zimmer and J. Kaufman and Q. T.
                      Le and A. J. Gentles and C. S. Kong and S. K. Plevritis and
                      Y. Goltsev and J. W. Hickey and G. P. Nolan},
      title        = {{L}ymph node colonization induces tissue remodeling via
                      immunosuppressive fibroblast-myeloid cell niches supporting
                      metastatic tolerance.},
      journal      = {Cancer cell},
      volume       = {nn},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2026-00256},
      pages        = {nn},
      year         = {2026},
      note         = {epub},
      abstract     = {Lymph node (LN) colonization in cancer is linked to poor
                      prognosis. Evidence suggests that LN colonization induces
                      systemic immunosuppression, facilitating distant metastasis.
                      We investigated LN-mediated immunosuppression in patients
                      with head-and-neck cancer using spatial proteomics, spatial
                      transcriptomics, and an in vivo model of melanoma LN
                      metastasis. Both primary tumors and paired LNs of
                      nodal-positive patients exhibit enhanced interferon-γ
                      signaling and an enrichment of immunosuppressive myeloid
                      cells and cancer-associated fibroblasts (CAFs). The spatial
                      intersection of these myeloid-CAF-enriched niches with
                      perifollicular T cell zones and LN follicles is linked to
                      enhanced T cell dysfunction and Treg activation therein,
                      thereby driving architectural LN remodeling. These immune
                      suppressive changes extend to adjacent non-tumor-involved LN
                      regions and nearby tumor-free LNs, but were not detected in
                      LNs of non-cancer patients, reflecting a systemic effect
                      that compromises anti-tumor immunity beyond the
                      tumor-involved LN. Hence, our findings establish LN
                      colonization as an active driver of systemic
                      immunosuppression, facilitating metastatic progression.},
      keywords     = {cancer-associated fibroblasts (Other) / head-and-neck
                      cancer (Other) / immunomodulation (Other) / lymph nodes
                      (Other) / metastasis (Other) / multiplex imaging (Other) /
                      spatial context (Other) / spatial transcriptomics (Other) /
                      tumor immune evasion (Other) / tumor microenvironment
                      (Other)},
      cin          = {A360},
      ddc          = {610},
      cid          = {I:(DE-He78)A360-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41616773},
      doi          = {10.1016/j.ccell.2026.01.003},
      url          = {https://inrepo02.dkfz.de/record/309606},
}