TY  - JOUR
AU  - de Boer, Rudolf A
AU  - Hulot, Jean-Sébastien
AU  - Gabriele Tocchetti, Carlo
AU  - Aboumsallem, Joseph Pierre
AU  - Ameri, Pietro
AU  - Anker, Stefan D
AU  - Bauersachs, Johann
AU  - Bertero, Edoardo
AU  - Coats, Andrew A J
AU  - Čelutkienė, Jelena
AU  - Chioncel, Ovidiu
AU  - Dodion, Pierre
AU  - Eschenhagen, Thomas
AU  - Farmakis, Dimitrios
AU  - Bayes-Genis, Antoni
AU  - Jäger, Dirk
AU  - Jankowska, Ewa A
AU  - Kitsis, Richard N
AU  - Konety, Suma H
AU  - Larkin, James
AU  - Lehmann, Lorenz
AU  - Lenihan, Daniel J
AU  - Maack, Christoph
AU  - Moslehi, Javid
AU  - Müller, Oliver J
AU  - Nowak-Sliwinska, Patrycja
AU  - Piepoli, Massimo Francesco
AU  - Ponikowski, Piotr
AU  - Pudil, Radek
AU  - Rainer, Peter P
AU  - Ruschitzka, Frank
AU  - Sawyer, Douglas
AU  - Seferovic, Petar M
AU  - Suter, Thomas
AU  - Thum, Thomas
AU  - van der Meer, Peter
AU  - Van Laake, Linda W
AU  - von Haehling, Stephan
AU  - Heymans, Stephane
AU  - Lyon, Alexander R
AU  - Backs, Johannes
TI  - Common Mechanistic Pathways in Cancer and Heart Failure.
JO  - European journal of heart failure
VL  - 22
IS  - 12
SN  - 1879-0844
CY  - Oxford
PB  - Wiley
M1  - DKFZ-2020-02269
SP  - 2272-2289
PY  - 2020
N1  - 2020 Dec;22(12):2272-2289
AB  - 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.
LB  - PUB:(DE-HGF)16
C6  - pmid:33094495
DO  - DOI:10.1002/ejhf.2029
UR  - https://inrepo02.dkfz.de/record/164129
ER  -