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@ARTICLE{Bartos:272724,
      author       = {Bartos, Laura M and Quach, Stefanie and Zenatti, Valerio
                      and Kirchleitner, Sabrina V and Blobner, Jens and Wind,
                      Karin and Kolabas, Zeynep Ilgin and Ulukaya, Selin and
                      Holzgreve, Adrien and Ruf, Viktoria C and Kunze, Lea and
                      Kunte, Sebastian T and Hoermann, Leonie and Härtel, Marlies
                      and Park, Ha Eun and Groß, Mattes and Franzmeier, Nicolai
                      and Zatcepin, Artem and Zounek, Adrian and Kaiser, Lena and
                      Riemenschneider, Markus J and Perneczky, Robert and
                      Rauchmann, Boris Stephan and Stöcklein, Sophia and Ziegler,
                      Sibylle and Herms, Jochen and Ertürk, Ali and Tonn, Joerg C
                      and Thon, Niklas and von Baumgarten, Louisa and Prestel,
                      Matthias and Tahirovic, Sabina and Albert, Nathalie L and
                      Brendel, Matthias},
      title        = {{R}emote {N}euroinflammation in {N}ewly {D}iagnosed
                      {G}lioblastoma {C}orrelates with {U}nfavorable {C}linical
                      {O}utcome.},
      journal      = {Clinical cancer research},
      volume       = {30},
      number       = {20},
      issn         = {1078-0432},
      address      = {Philadelphia, Pa. [u.a.]},
      publisher    = {AACR},
      reportid     = {DZNE-2024-01226},
      pages        = {4618 - 4634},
      year         = {2024},
      abstract     = {Current therapy strategies still provide only limited
                      success in the treatment of glioblastoma, the most frequent
                      primary brain tumor in adults. In addition to the
                      characterization of the tumor microenvironment, global
                      changes in the brain of patients with glioblastoma have been
                      described. However, the impact and molecular signature of
                      neuroinflammation distant of the primary tumor site have not
                      yet been thoroughly elucidated.We performed translocator
                      protein (TSPO)-PET in patients with newly diagnosed
                      glioblastoma (n = 41), astrocytoma WHO grade 2 (n = 7), and
                      healthy controls (n = 20) and compared TSPO-PET signals of
                      the non-lesion (i.e., contralateral) hemisphere.
                      Back-translation into syngeneic SB28 glioblastoma mice was
                      used to characterize Pet alterations on a cellular level.
                      Ultimately, multiplex gene expression analyses served to
                      profile immune cells in remote brain.Our study revealed
                      elevated TSPO-PET signals in contralateral hemispheres of
                      patients with newly diagnosed glioblastoma compared to
                      healthy controls. Contralateral TSPO was associated with
                      persisting epileptic seizures and shorter overall survival
                      independent of the tumor phenotype. Back-translation into
                      syngeneic glioblastoma mice pinpointed myeloid cells as the
                      predominant source of contralateral TSPO-PET signal
                      increases and identified a complex immune signature
                      characterized by myeloid cell activation and
                      immunosuppression in distant brain regions.Neuroinflammation
                      within the contralateral hemisphere can be detected with
                      TSPO-PET imaging and associates with poor outcome in
                      patients with newly diagnosed glioblastoma. The molecular
                      signature of remote neuroinflammation promotes the
                      evaluation of immunomodulatory strategies in patients with
                      detrimental whole brain inflammation as reflected by high
                      TSPO expression.},
      keywords     = {Glioblastoma: pathology / Glioblastoma: genetics /
                      Glioblastoma: metabolism / Glioblastoma: diagnosis /
                      Glioblastoma: mortality / Humans / Animals / Mice /
                      Receptors, GABA: metabolism / Receptors, GABA: genetics /
                      Male / Female / Middle Aged / Brain Neoplasms: pathology /
                      Brain Neoplasms: genetics / Brain Neoplasms: metabolism /
                      Brain Neoplasms: diagnosis / Neuroinflammatory Diseases:
                      pathology / Neuroinflammatory Diseases: etiology /
                      Neuroinflammatory Diseases: diagnosis / Adult /
                      Positron-Emission Tomography: methods / Aged / Prognosis /
                      Tumor Microenvironment: immunology / Disease Models, Animal
                      / Receptors, GABA (NLM Chemicals) / TSPO protein, human (NLM
                      Chemicals)},
      cin          = {AG Haass / AG Tahirovic / AG Dichgans / AG Herms},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007 / I:(DE-2719)1140003 /
                      I:(DE-2719)5000022 / I:(DE-2719)1110001},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39150564},
      pmc          = {pmc:PMC11474166},
      doi          = {10.1158/1078-0432.CCR-24-1563},
      url          = {https://pub.dzne.de/record/272724},
}