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@ARTICLE{Liebig:210389,
      author       = {S. Liebig and M. Neumann$^*$ and P. Silva and J.
                      Ortiz-Tanchez and V. Schulze and K. Isaakidis and C. Schlee
                      and M. P. Schroeder and T. Beder and L. G. T. Morris and T.
                      A. Chan and L. Bastian$^*$ and T. Burmeister and S. Schwartz
                      and N. Gökbuget$^*$ and L. H. Mochmann and C. D.
                      Baldus$^*$},
      title        = {{FAT}1 expression in {T}-cell acute lymphoblastic leukemia
                      ({T}-{ALL}) modulates proliferation and {WNT} signaling.},
      journal      = {Scientific reports},
      volume       = {13},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2023-00118},
      pages        = {972},
      year         = {2023},
      abstract     = {FAT atypical cadherin 1 (FAT1), a transmembrane protein, is
                      frequently mutated in various cancer types and has been
                      described as context-dependent tumor suppressor or oncogene.
                      The FAT1 gene is mutated in $12-16\%$ of T-cell acute
                      leukemia (T-ALL) and aberrantly expressed in about $54\%$ of
                      T-ALL cases contrasted with absent expression in normal
                      T-cells. Here, we characterized FAT1 expression and profiled
                      the methylation status from T-ALL patients. In our T-ALL
                      cohort, $53\%$ of patient samples were FAT1 positive
                      (FAT1pos) compared to only $16\%$ FAT1 positivity in early
                      T-ALL patient samples. Aberrant expression of FAT1 was
                      strongly associated with FAT1 promotor hypomethylation, yet
                      a subset, mainly consisting of TLX1-driven T-ALL patient
                      samples showed methylation-independent high FAT1 expression.
                      Genes correlating with FAT1 expression revealed enrichment
                      in WNT signaling genes representing the most enriched single
                      pathway. FAT1 knockdown or knockout led to impaired
                      proliferation and downregulation of WNT pathway target genes
                      (CCND1, MYC, LEF1), while FAT1 overexpressing conveyed a
                      proliferative advantage. To conclude, we characterized a
                      subtype pattern of FAT1 gene expression in adult T-ALL
                      patients correlating with promotor methylation status. FAT1
                      dependent proliferation and WNT signaling discloses an
                      impact on deeper understanding of T-ALL leukemogenesis as a
                      fundament for prospective therapeutic strategies.},
      cin          = {FM01 / BE01},
      ddc          = {600},
      cid          = {I:(DE-He78)FM01-20160331 / I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36653435},
      doi          = {10.1038/s41598-023-27792-0},
      url          = {https://inrepo02.dkfz.de/record/210389},
}