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@ARTICLE{Ahadova:182209,
      author       = {A. Ahadova$^*$ and J. Witt$^*$ and S. Haupt and R. Gallon
                      and R. Hüneburg and J. Nattermann and S. Ten Broeke and L.
                      Bohaumilitzky$^*$ and A. Hernandez-Sanchez$^*$ and M.
                      Santibanez-Koref and M. S. Jackson and M. Ahtiainen and K.
                      Pylvänäinen and K. Andini and V. K. Grolmusz and G.
                      Möslein and M. Dominguez-Valentin and P. Møller and D.
                      Fürst and R. Sijmons and G. M. Borthwick and J. Burn and
                      J.-P. Mecklin and V. Heuveline and M. von Knebel
                      Doeberitz$^*$ and T. Seppälä and M. Kloor$^*$},
      title        = {{I}s {HLA} type a possible cancer risk modifier in {L}ynch
                      syndrome?},
      journal      = {International journal of cancer},
      volume       = {152},
      number       = {10},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2022-02503},
      pages        = {2024-2031},
      year         = {2023},
      note         = {#EA:F210#LA:F210# / 2023 May 15;152(10):2024-2031},
      abstract     = {Lynch syndrome (LS) is the most common inherited cancer
                      syndrome. It is inherited via a monoallelic germline variant
                      in one of the DNA mismatch repair (MMR) genes. LS carriers
                      have a broad $30\%$ to $80\%$ risk of developing various
                      malignancies, and more precise, individual risk estimations
                      would be of high clinical value, allowing tailored cancer
                      prevention and surveillance. Due to MMR deficiency, LS
                      cancers are characterized by the accumulation of frameshift
                      mutations leading to highly immunogenic frameshift peptides
                      (FSPs). Thus, immune surveillance is proposed to inhibit the
                      outgrowth of MMR-deficient cell clones. Recent studies have
                      shown that immunoediting during the evolution of
                      MMR-deficient cancers leads to a counter-selection of highly
                      immunogenic antigens. The immunogenicity of FSPs is
                      dependent on the antigen presentation. One crucial factor
                      determining antigen presentation is the HLA genotype. Hence,
                      a LS carrier's HLA genotype plays an important role in the
                      presentation of FSP antigens to the immune system, and may
                      influence the likelihood of progression from precancerous
                      lesions to cancer. To address the challenge of clarifying
                      this possibility including diverse populations with
                      different HLA types, we have established the INDICATE
                      initiative (Individual cancer risk by HLA type,
                      http://indicate-lynch.org/), an international network aiming
                      at a systematic evaluation of the HLA genotype as a possible
                      cancer risk modifier in LS. Here we summarize the current
                      knowledge on the role of HLA type in cancer risk and outline
                      future research directions to delineate possible association
                      in the scenario of LS with genetically defined risk
                      population and highly immunogenic tumors.},
      subtyp        = {Review Article},
      keywords     = {HLA genotype (Other) / Lynch syndrome (Other) / cancer
                      immunoediting (Other) / immune surveillance (Other) /
                      personalized cancer risk (Other)},
      cin          = {F210},
      ddc          = {610},
      cid          = {I:(DE-He78)F210-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36214792},
      doi          = {10.1002/ijc.34312},
      url          = {https://inrepo02.dkfz.de/record/182209},
}