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@ARTICLE{Parikh:290080,
      author       = {R. Parikh and S. Parikh and D. Berzin and H. Vaknine and S.
                      Ovadia and D. Likonen and S. Greenberger and A. Scope and S.
                      Elgavish and Y. Nevo and I. Plaschkes and E. Nizri and O.
                      Kobiler and A. Maliah and L. Zaremba$^*$ and V. Mohan and I.
                      Sagi and R. Ashery-Padan and Y. Carmi and C. Luxenburg and
                      J. Hoheisel$^*$ and M. Khaled and M. P. Levesque and C.
                      Levy},
      title        = {{R}ecycled melanoma-secreted melanosomes regulate
                      tumor-associated macrophage diversification.},
      journal      = {The EMBO journal},
      volume       = {43},
      number       = {17},
      issn         = {0261-4189},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2024-00979},
      pages        = {3553-3586},
      year         = {2024},
      note         = {2024 Sep;43(17):3553-3586},
      abstract     = {Extracellular vesicles (EVs) are important mediators of
                      communication between cells. Here, we reveal a new mode of
                      intercellular communication by melanosomes, large EVs
                      secreted by melanocytes for melanin transport. Unlike small
                      EVs, which are disintegrated within the receiver cell,
                      melanosomes stay intact within them, gain a unique protein
                      signature, and can then be further transferred to another
                      cell as 'second-hand' EVs. We show that melanoma-secreted
                      melanosomes passaged through epidermal keratinocytes or
                      dermal fibroblasts can be further engulfed by resident
                      macrophages. This process leads to macrophage polarization
                      into pro-tumor or pro-immune cell infiltration phenotypes.
                      Melanosomes that are transferred through fibroblasts can
                      carry AKT1, which induces VEGF secretion from macrophages in
                      an mTOR-dependent manner, promoting angiogenesis and
                      metastasis in vivo. In melanoma patients, macrophages that
                      are co-localized with AKT1 are correlated with disease
                      aggressiveness, and immunotherapy non-responders are
                      enriched in macrophages containing melanosome markers. Our
                      findings suggest that interactions mediated by second-hand
                      extracellular vesicles contribute to the formation of the
                      metastatic niche, and that blocking the melanosome cues of
                      macrophage diversification could be helpful in halting
                      melanoma progression.},
      keywords     = {Angiogenesis (Other) / Cell-to-Cell-Transfer (Other) /
                      Heterogeneity (Other) / Melanosomes (Other) / Tumor
                      Associated Macrophages (Other)},
      cin          = {B070},
      ddc          = {570},
      cid          = {I:(DE-He78)B070-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38719996},
      doi          = {10.1038/s44318-024-00103-7},
      url          = {https://inrepo02.dkfz.de/record/290080},
}