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@ARTICLE{deBoer:164129,
      author       = {R. A. de Boer and J.-S. Hulot and C. Gabriele Tocchetti and
                      J. P. Aboumsallem and P. Ameri and S. D. Anker and J.
                      Bauersachs and E. Bertero and A. A. J. Coats and J.
                      Čelutkienė and O. Chioncel and P. Dodion and T.
                      Eschenhagen and D. Farmakis and A. Bayes-Genis and D. Jäger
                      and E. A. Jankowska and R. N. Kitsis and S. H. Konety and J.
                      Larkin and L. Lehmann$^*$ and D. J. Lenihan and C. Maack and
                      J. Moslehi and O. J. Müller and P. Nowak-Sliwinska and M.
                      F. Piepoli and P. Ponikowski and R. Pudil and P. P. Rainer
                      and F. Ruschitzka and D. Sawyer and P. M. Seferovic and T.
                      Suter and T. Thum and P. van der Meer and L. W. Van Laake
                      and S. von Haehling and S. Heymans and A. R. Lyon and J.
                      Backs},
      title        = {{C}ommon {M}echanistic {P}athways in {C}ancer and {H}eart
                      {F}ailure.},
      journal      = {European journal of heart failure},
      volume       = {22},
      number       = {12},
      issn         = {1879-0844},
      address      = {Oxford},
      publisher    = {Wiley},
      reportid     = {DKFZ-2020-02269},
      pages        = {2272-2289},
      year         = {2020},
      note         = {2020 Dec;22(12):2272-2289},
      abstract     = {The co-occurrence of cancer and heart failure (HF)
                      represents a significant clinical drawback as each disease
                      interferes with the treatment of the other. In addition to
                      shared risk factors, a growing body of experimental and
                      clinical evidence reveals numerous commonalities in the
                      biology underlying both pathologies. Inflammation emerges as
                      a common hallmark for both diseases as it contributes to the
                      initiation, and progression of both HF and cancer. Under
                      stress, malignant and cardiac cells change their metabolic
                      preferences to survive, which makes these metabolic
                      derangements a great basis to develop intersection
                      strategies and therapies to combat both diseases. Further,
                      genetic predisposition and clonal hematopoiesis are common
                      drivers for both conditions and they hold great clinical
                      relevance in the context of personalized medicine. Also,
                      altered angiogenesis is a common hallmark for failing hearts
                      and tumors and represents a promising substrate to target in
                      both diseases. Cardiac cells and malignant cells interact
                      with their surrounding environment called stroma. This
                      interaction mediates the progression of the 2 pathologies
                      and understanding the structure and function of each stromal
                      component may pave the way for innovative therapeutic
                      strategies and improved outcomes in patients. The
                      interdisciplinary collaboration between cardiologists and
                      oncologists is essential to establish unified guidelines.
                      Also, preclinical models that mimic the human situation,
                      where both pathologies coexist, are needed to understand all
                      the aspects of the bidirectional relationship between cancer
                      and HF. Finally, adequately powered clinical studies,
                      including all ages, and men and women, with proper
                      adjudication of both cancer and CV end points, are essential
                      to accurately study these two pathologies at the same time.},
      cin          = {G834},
      ddc          = {610},
      cid          = {I:(DE-He78)G834-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33094495},
      doi          = {10.1002/ejhf.2029},
      url          = {https://inrepo02.dkfz.de/record/164129},
}