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@ARTICLE{Zou:303449,
      author       = {X. Zou and S. Nie and J. Cao and M. Shi and K. Schuck and
                      Z. Shi and L. Zhang and H. Li and Y. Sun and C. Fang and J.
                      Hu and Y. Niu and Y. Yu and Z. Zhang and C. Li and M. Hu and
                      L. Wang and K. Jiang and Z. Lu and J. Akkan and S. Raulefs
                      and C. Kahlert and S. Roth and I. Herr and Y. Wan and A.
                      Mihaljevic and X. Qian and Q. Zhang and M. H. Wang and J.
                      Kleeff and H. Friess and Z. Gu$^*$ and C. W. Michalski and
                      S. Shen and B. Kong},
      title        = {{ALDH}1{A}3 promotes aggressive basal-like pancreatic
                      cancer through an {AP}-1/{RUNX}2 enhancer network.},
      journal      = {Oncogene},
      volume       = {nn},
      issn         = {0950-9232},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01662},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {The basal-like transcriptional subtype of pancreatic ductal
                      adenocarcinoma (PDAC) is linked to therapy resistance and
                      poor prognosis. The cancer stem cell marker aldehyde
                      dehydrogenase 1A3 (ALDH1A3) is a critical enzyme in
                      acetaldehyde metabolism, but the interconnection to the
                      basal-like subtype is poorly understood. Here, we identified
                      ALDH1A3 as a key gene, which correlates with reduced
                      survival and increased tumor growth. Functional studies
                      revealed interaction of ALDH1A3 with genes like FAM3C, MCC,
                      PMEPA1, and IRS2, forming a network driving PDAC
                      progression. Chromatin profiling showed that ALDH1A3 affects
                      acetylation of histone 3, mediating AP-1 activity,
                      particularly via FOS family members, activating oncogenic
                      pathways such as MAPK and TNF signaling. RUNX2 emerged as a
                      therapeutic target within this network, as its knockdown
                      disrupted MAPK signaling and reduced tumor growth. These
                      findings emphasize the role of ALDH1A3 in linking nuclear
                      metabolic-epigenetic programming in basal-like PDAC,
                      highlighting it as a promising therapeutic target for novel
                      treatment strategies.},
      cin          = {W610},
      ddc          = {610},
      cid          = {I:(DE-He78)W610-20160331},
      pnm          = {319H - Addenda (POF4-319H)},
      pid          = {G:(DE-HGF)POF4-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40781158},
      doi          = {10.1038/s41388-025-03530-w},
      url          = {https://inrepo02.dkfz.de/record/303449},
}