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@ARTICLE{Kinzler:301293,
      author       = {M. N. Kinzler and E. Metzger$^*$ and R. Schulz and K.
                      Bankov and A. Ramos-Triguero and F. Schulze and S. Gretser
                      and N. Abedin and A. Wiegering and S. Zeuzem and D. Walter
                      and H. Reis and R. Schüle$^*$ and P. J. Wild},
      title        = {{O}verexpression of {KMT}9α is associated with poor
                      outcome in cholangiocarcinoma patients.},
      journal      = {Journal of cancer research and clinical oncology},
      volume       = {151},
      number       = {5},
      issn         = {0301-1585},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DKFZ-2025-00977},
      pages        = {161},
      year         = {2025},
      abstract     = {The newly discovered histone methyltransferase KMT9 serves
                      as an epigenetic regulator of carcinogenesis in various
                      cancer entities. For the first time, we investigated the
                      presence of KMT9α in cholangiocarcinoma, the association
                      with histologic subtypes, and its impact on survival.A
                      tissue microarray cohort of all CCA patients who underwent
                      surgical resection with curative intent between 08/2005 and
                      12/2021 at the University Hospital Frankfurt was
                      immunohistochemically analyzed with the KMT9α antibody. For
                      overall survival, Kaplan-Meier curves and Cox-regression
                      analyses were performed.In total, 174 patients were suitable
                      for IHC analysis. Of the patients, $35.1\%$ (n = 61)
                      overexpressed KMT9α. Kaplan-Meier curves revealed a median
                      OS of 34.75 months $(95\%$ CI = 20.23-49.27 months) for all
                      CCA patients positive for KMT9α in comparison to 54.21
                      months $(95\%$ CI = 41.78-66.63 months) for patients lacking
                      KMT9α overexpression (p = 0.004). Subtype analysis revealed
                      strong differences in KMT9α expression. Multivariate Cox
                      regression analysis identified KMT9α as an independent risk
                      factor for shorter OS in CCA.This study demonstrates that a
                      marked subset of CCA patients exhibit overexpression of
                      KMT9α. These findings underscore the prognostic
                      significance of KMT9α and reinforce its potential as a
                      therapeutic target, consistent with its role in other cancer
                      types.},
      keywords     = {Humans / Cholangiocarcinoma: pathology /
                      Cholangiocarcinoma: mortality / Cholangiocarcinoma:
                      enzymology / Cholangiocarcinoma: genetics /
                      Cholangiocarcinoma: metabolism / Cholangiocarcinoma: surgery
                      / Male / Histone-Lysine N-Methyltransferase: biosynthesis /
                      Histone-Lysine N-Methyltransferase: metabolism /
                      Histone-Lysine N-Methyltransferase: genetics / Female / Bile
                      Duct Neoplasms: pathology / Bile Duct Neoplasms: mortality /
                      Bile Duct Neoplasms: enzymology / Bile Duct Neoplasms:
                      metabolism / Bile Duct Neoplasms: genetics / Bile Duct
                      Neoplasms: surgery / Middle Aged / Aged / Adult / Prognosis
                      / Biomarkers, Tumor: metabolism / Aged, 80 and over /
                      Kaplan-Meier Estimate / Tissue Array Analysis / Biomarker
                      (Other) / Cholangiocarcinoma (Other) / KMT9α (Other) /
                      Lysine methyltransferase 9 (Other) / Surgical oncology
                      (Other) / Histone-Lysine N-Methyltransferase (NLM Chemicals)
                      / Biomarkers, Tumor (NLM Chemicals)},
      cin          = {FR01},
      ddc          = {610},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40355770},
      doi          = {10.1007/s00432-025-06214-w},
      url          = {https://inrepo02.dkfz.de/record/301293},
}