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@ARTICLE{Horvat:289486,
      author       = {N. K. Horvat and S. Chocarro$^*$ and O. Marques and T. A.
                      Bauer and R. Qiu and A. Diaz-Jimenez$^*$ and B. Helm$^*$ and
                      Y. Chen$^*$ and S. Sawall$^*$ and R. Sparla and L. Su and U.
                      Klingmüller$^*$ and M. Barz and M. W. Hentze and R.
                      Sotillo$^*$ and M. U. Muckenthaler},
      title        = {{S}uperparamagnetic {I}ron {O}xide {N}anoparticles
                      {R}eprogram the {T}umor {M}icroenvironment and {R}educe
                      {L}ung {C}ancer {R}egrowth after {C}rizotinib {T}reatment.},
      journal      = {ACS nano},
      volume       = {18},
      number       = {17},
      issn         = {1936-0851},
      address      = {Washington, DC},
      publisher    = {Soc.},
      reportid     = {DKFZ-2024-00808},
      pages        = {11025-11041},
      year         = {2024},
      note         = {#LA:B220# / 2024 Apr 30;18(17):11025-11041},
      abstract     = {ALK-positive NSCLC patients demonstrate initial responses
                      to ALK tyrosine kinase inhibitor (TKI) treatments, but
                      eventually develop resistance, causing rapid tumor relapse
                      and poor survival rates. Growing evidence suggests that the
                      combination of drug and immune therapies greatly improves
                      patient survival; however, due to the low immunogenicity of
                      the tumors, ALK-positive patients do not respond to
                      currently available immunotherapies. Tumor-associated
                      macrophages (TAMs) play a crucial role in facilitating lung
                      cancer growth by suppressing tumoricidal immune activation
                      and absorbing chemotherapeutics. However, they can also be
                      programmed toward a pro-inflammatory tumor suppressive
                      phenotype, which represents a highly active area of therapy
                      development. Iron loading of TAMs can achieve such
                      reprogramming correlating with an improved prognosis in lung
                      cancer patients. We previously showed that superparamagnetic
                      iron oxide nanoparticles containing core-cross-linked
                      polymer micelles (SPION-CCPMs) target macrophages and
                      stimulate pro-inflammatory activation. Here, we show that
                      SPION-CCPMs stimulate TAMs to secrete reactive nitrogen
                      species and cytokines that exert tumoricidal activity. We
                      further show that SPION-CCPMs reshape the immunosuppressive
                      Eml4-Alk lung tumor microenvironment (TME) toward a
                      cytotoxic profile hallmarked by the recruitment of CD8+ T
                      cells, suggesting a multifactorial benefit of SPION-CCPM
                      application. When intratracheally instilled into lung
                      cancer-bearing mice, SPION-CCPMs delay tumor growth and,
                      after first line therapy with a TKI, halt the regrowth of
                      relapsing tumors. These findings identify SPIONs-CCPMs as an
                      adjuvant therapy, which remodels the TME, resulting in a
                      delay in the appearance of resistant tumors.},
      keywords     = {adjuvant therapy (Other) / iron homeostasis (Other) / lung
                      cancer (Other) / nanoparticle (Other) / polymeric micelle
                      (Other)},
      cin          = {B220 / HD01 / B200 / E025},
      ddc          = {540},
      cid          = {I:(DE-He78)B220-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B200-20160331 / I:(DE-He78)E025-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38626916},
      doi          = {10.1021/acsnano.3c08335},
      url          = {https://inrepo02.dkfz.de/record/289486},
}