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@ARTICLE{Ahmad:288068,
      author       = {O. Ahmad$^*$ and T. Ahmad and S. Pfister$^*$},
      title        = {{IDH} mutation, glioma immunogenicity, and therapeutic
                      challenge of primary mismatch repair deficient {IDH}-mutant
                      astrocytoma {PMMRDIA}: a systematic review.},
      journal      = {Molecular oncology},
      volume       = {18},
      number       = {12},
      issn         = {1574-7891},
      address      = {Hoboken, NJ},
      publisher    = {John Wiley $\&$ Sons, Inc.},
      reportid     = {DKFZ-2024-00326},
      pages        = {2822-2841},
      year         = {2024},
      note         = {2024 Dec;18(12):2822-2841 / #EA:B062#LA:B062#},
      abstract     = {In 2021, Suwala et al. described Primary Mismatch Repair
                      Deficient IDH-mutant Astrocytoma (PMMRDIA) as a distinct
                      group of gliomas. In unsupervised clustering, PMMRDIA forms
                      distinct cluster, separate from other IDH-mutant gliomas,
                      including IDH-mutant gliomas with secondary mismatch repair
                      (MMR) deficiency. In the published cohort, three patients
                      received treatment with an immune checkpoint blocker (ICB),
                      yet none exhibited a response, which aligns with existing
                      knowledge about the decreased immunogenicity of IDH-mutant
                      gliomas in comparison to IDH-wildtype. In the case of
                      PMMRDIA, the inherent resistance to the standard-of-care
                      temozolomide caused by MMR deficiency is an additional
                      challenge. It is known that a gain-of-function mutation of
                      IDH1/2 genes produces the oncometabolite
                      R-2-hydroxyglutarate (R-2-HG), which increases DNA and
                      histone methylation contributing to the characteristic
                      glioma-associated CpG island methylator phenotype (G-CIMP).
                      While other factors could be involved in remodeling the
                      tumor microenvironment (TME) of IDH-mutant gliomas, this
                      systematic review emphasizes the role of R-2-HG and the
                      subsequent G-CIMP in immune suppression. This highlights a
                      potential actionable pathway to enhance the response of ICB,
                      which might be relevant for addressing the unmet therapeutic
                      challenge of PMMRDIA.},
      subtyp        = {Review Article},
      keywords     = {IDH-mutant glioma (Other) / PMMRDIA (Other) /
                      immunogenicity (Other)},
      cin          = {B062 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38339779},
      doi          = {10.1002/1878-0261.13598},
      url          = {https://inrepo02.dkfz.de/record/288068},
}