% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Kbler:304084,
      author       = {K. Kübler$^*$ and A. Nardone and S. Anand and D. Gurevich
                      and J. Gao and M. Droog and F. Hermida-Prado and T. Akhshi
                      and A. Feiglin and A. S. Feit and G. Cohen Feit and G.
                      Dackus and M. Pun and Y. Kuang and J. Cha and M. Miller and
                      S. Gregoricchio and M. Lanfermeijer and S. Cornelissen and
                      W. J. Gibson and C. P. Paweletz and E. M. Van Allen and F.
                      E. van Leeuwen and P. M. Nederlof and Q.-D. Nguyen and M. J.
                      E. Mourits and M. Radovich and I. Leshchiner and C. Stewart
                      and U. A. Matulonis and W. Zwart and Y. E. Maruvka and G.
                      Getz and R. Jeselsohn},
      title        = {{T}amoxifen induces {PI}3{K} activation in uterine cancer.},
      journal      = {Nature genetics},
      volume       = {57},
      number       = {9},
      issn         = {1061-4036},
      address      = {London},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2025-01752},
      pages        = {2192-2202},
      year         = {2025},
      note         = {2025 Sep;57(9):2192-2202},
      abstract     = {Mutagenic processes and clonal selection contribute to the
                      development of therapy-associated secondary neoplasms, a
                      known complication of cancer treatment. The association
                      between tamoxifen therapy and secondary uterine cancers is
                      uncommon but well established; however, the genetic
                      mechanisms underlying tamoxifen-driven tumorigenesis remain
                      unclear. We find that oncogenic PIK3CA mutations, common in
                      spontaneously arising estrogen-associated de novo uterine
                      cancer, are significantly less frequent in
                      tamoxifen-associated tumors. In vivo, tamoxifen-induced
                      estrogen receptor stimulation activates phosphoinositide
                      3-kinase (PI3K) signaling in normal mouse uterine tissue,
                      potentially eliminating the selective benefit of
                      PI3K-activating mutations in tamoxifen-associated uterine
                      cancer. Together, we present a unique pathway of
                      therapy-associated carcinogenesis in which tamoxifen-induced
                      activation of the PI3K pathway acts as a non-genetic driver
                      event, contributing to the multistep model of uterine
                      carcinogenesis. While this PI3K mechanism is specific to
                      tamoxifen-associated uterine cancer, the concept of
                      treatment-induced signaling events may have broader
                      applicability to other routes of tumorigenesis.},
      cin          = {BE01},
      ddc          = {570},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40846762},
      doi          = {10.1038/s41588-025-02308-w},
      url          = {https://inrepo02.dkfz.de/record/304084},
}