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@ARTICLE{Balzasch:309998,
      author       = {B. M. Balzasch and A. von Kries and S. Hüll and I. A.
                      Shaltiel and K. E. Boonekamp$^*$ and V. Ast and E.
                      Burgermeister and J. Betge$^*$ and M. Ebert and M.
                      Boutros$^*$ and L. Helming and V. Umansky$^*$ and A.
                      Cerwenka},
      title        = {{M}onocytes acquire a tumor-associated {IL}1{B} program
                      upon encountering patient-derived colon cancer organoids.},
      journal      = {OncoImmunology},
      volume       = {15},
      number       = {1},
      issn         = {2162-4011},
      address      = {Abingdon},
      publisher    = {Taylor $\&$ Franics},
      reportid     = {DKFZ-2026-00411},
      pages        = {2633012},
      year         = {2026},
      abstract     = {Tumor-associated macrophages (TAMs) and monocytes that
                      accumulate in colorectal cancer (CRC) play a crucial role in
                      shaping the tumor microenvironment (TME) and anti-tumor
                      immune responses. Although TAMs have been linked to both
                      pro- and anti-tumor functions, our understanding of the cues
                      instructing their heterogeneous phenotypes and function in
                      cancer patients remains limited. Here, we established
                      co-cultures comprising primary human monocytes and
                      patient-derived organoids (PDOs) from patients with
                      microsatellite-stable CRC to emulate myeloid/tumor cell
                      interactions in vitro. Upon encountering PDOs, monocytes
                      acquire phenotypic changes that are distinct from those
                      induced by typical polarization protocols. Single-cell RNA
                      sequencing revealed that PDO-exposed monocytes
                      transcriptionally resembled IL1B-programmed monocytes
                      previously identified in the tumor tissues of CRC patients.
                      This phenotype emerged independently of tumor mutational
                      profiles or consensus molecular subtypes. Mechanistically,
                      soluble PDO-derived mediators induced the production of
                      CXCL2, CXCL5 and CXCL7 chemokines, whereas the phagocytic
                      uptake of tumor debris impaired the MHC class II-mediated
                      antigen presentation capabilities of monocytes in
                      co-culture. In addition, our in vitro system allowed
                      functional assessment of PDO-exposed monocytes demonstrating
                      a compromised capacity to mount an inflammatory response
                      upon TLR stimulation. Together, PDO-monocyte co-cultures
                      offer a platform to dissect the interplay between cancer
                      cells and monocytes, and advance our understanding of
                      myeloid plasticity and function in cancer patients.},
      keywords     = {Humans / Organoids: pathology / Organoids: immunology /
                      Organoids: metabolism / Monocytes: immunology / Monocytes:
                      metabolism / Monocytes: pathology / Interleukin-1beta:
                      metabolism / Colonic Neoplasms: pathology / Colonic
                      Neoplasms: immunology / Colonic Neoplasms: metabolism /
                      Colonic Neoplasms: genetics / Tumor Microenvironment:
                      immunology / Coculture Techniques / Tumor-Associated
                      Macrophages: immunology / Tumor-Associated Macrophages:
                      metabolism / IL1B (Other) / Organoid (Other) / colon cancer
                      (Other) / tumor-associated macrophages (Other) /
                      Interleukin-1beta (NLM Chemicals) / IL1B protein, human (NLM
                      Chemicals)},
      cin          = {B110 / B440 / A370},
      ddc          = {610},
      cid          = {I:(DE-He78)B110-20160331 / I:(DE-He78)B440-20160331 /
                      I:(DE-He78)A370-20160331},
      pnm          = {319H - Addenda (POF4-319H)},
      pid          = {G:(DE-HGF)POF4-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41723598},
      doi          = {10.1080/2162402X.2026.2633012},
      url          = {https://inrepo02.dkfz.de/record/309998},
}