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@ARTICLE{Hassin:286387,
      author       = {O. Hassin and M. Sernik and A. Seligman and F. C. E.
                      Vogel$^*$ and M. D. Wellenstein and J. Smollich and C.
                      Halperin and A. C. Pirona and L. N. Toledano and C. D.
                      Caballero$^*$ and L. Schlicker$^*$ and T.-M. Salame and A.
                      Sarusi Portuguez and Y. Aylon and R. Scherz-Shouval and T.
                      Geiger and K. E. de Visser and A. Schulze$^*$ and M. Oren},
      title        = {p53 deficient breast cancer cells reprogram preadipocytes
                      toward tumor-protective immunomodulatory cells.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {120},
      number       = {52},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2023-02790},
      pages        = {e2311460120},
      year         = {2023},
      abstract     = {The TP53 gene is mutated in approximately $30\%$ of all
                      breast cancer cases. Adipocytes and preadipocytes, which
                      constitute a substantial fraction of the stroma of normal
                      mammary tissue and breast tumors, undergo transcriptional,
                      metabolic, and phenotypic reprogramming during breast cancer
                      development and play an important role in tumor progression.
                      We report here that p53 loss in breast cancer cells
                      facilitates the reprogramming of preadipocytes, inducing
                      them to acquire a unique transcriptional and metabolic
                      program that combines impaired adipocytic differentiation
                      with augmented cytokine expression. This, in turn, promotes
                      the establishment of an inflammatory tumor microenvironment,
                      including increased abundance of Ly6C+ and Ly6G+ myeloid
                      cells and elevated expression of the immune checkpoint
                      ligand PD-L1. We also describe a potential gain-of-function
                      effect of common p53 missense mutations on the inflammatory
                      reprogramming of preadipocytes. Altogether, our study
                      implicates p53 deregulation in breast cancer cells as a
                      driver of tumor-supportive adipose tissue reprogramming,
                      expanding the network of non-cell autonomous mechanisms
                      whereby p53 dysfunction may promote cancer. Further
                      elucidation of the interplay between p53 and adipocytes
                      within the tumor microenvironment may suggest effective
                      therapeutic targets for the treatment of breast cancer
                      patients.},
      keywords     = {adipocytes (Other) / breast cancer (Other) / p53 (Other) /
                      preadipocytes (Other)},
      cin          = {A410},
      ddc          = {500},
      cid          = {I:(DE-He78)A410-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38127986},
      doi          = {10.1073/pnas.2311460120},
      url          = {https://inrepo02.dkfz.de/record/286387},
}