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000164129 1001_ $$ade Boer, Rudolf A$$b0
000164129 245__ $$aCommon Mechanistic Pathways in Cancer and Heart Failure.
000164129 260__ $$aOxford$$bWiley$$c2020
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000164129 500__ $$a2020 Dec;22(12):2272-2289
000164129 520__ $$aThe 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.
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000164129 7001_ $$aHulot, Jean-Sébastien$$b1
000164129 7001_ $$aGabriele Tocchetti, Carlo$$b2
000164129 7001_ $$aAboumsallem, Joseph Pierre$$b3
000164129 7001_ $$aAmeri, Pietro$$b4
000164129 7001_ $$aAnker, Stefan D$$b5
000164129 7001_ $$aBauersachs, Johann$$b6
000164129 7001_ $$aBertero, Edoardo$$b7
000164129 7001_ $$aCoats, Andrew A J$$b8
000164129 7001_ $$aČelutkienė, Jelena$$b9
000164129 7001_ $$aChioncel, Ovidiu$$b10
000164129 7001_ $$aDodion, Pierre$$b11
000164129 7001_ $$aEschenhagen, Thomas$$b12
000164129 7001_ $$aFarmakis, Dimitrios$$b13
000164129 7001_ $$aBayes-Genis, Antoni$$b14
000164129 7001_ $$aJäger, Dirk$$b15
000164129 7001_ $$aJankowska, Ewa A$$b16
000164129 7001_ $$aKitsis, Richard N$$b17
000164129 7001_ $$aKonety, Suma H$$b18
000164129 7001_ $$aLarkin, James$$b19
000164129 7001_ $$0P:(DE-He78)2e191ef76e61b3bbc6de8657da38f2f7$$aLehmann, Lorenz$$b20$$udkfz
000164129 7001_ $$aLenihan, Daniel J$$b21
000164129 7001_ $$aMaack, Christoph$$b22
000164129 7001_ $$aMoslehi, Javid$$b23
000164129 7001_ $$aMüller, Oliver J$$b24
000164129 7001_ $$aNowak-Sliwinska, Patrycja$$b25
000164129 7001_ $$aPiepoli, Massimo Francesco$$b26
000164129 7001_ $$aPonikowski, Piotr$$b27
000164129 7001_ $$aPudil, Radek$$b28
000164129 7001_ $$aRainer, Peter P$$b29
000164129 7001_ $$aRuschitzka, Frank$$b30
000164129 7001_ $$aSawyer, Douglas$$b31
000164129 7001_ $$aSeferovic, Petar M$$b32
000164129 7001_ $$aSuter, Thomas$$b33
000164129 7001_ $$aThum, Thomas$$b34
000164129 7001_ $$avan der Meer, Peter$$b35
000164129 7001_ $$aVan Laake, Linda W$$b36
000164129 7001_ $$avon Haehling, Stephan$$b37
000164129 7001_ $$aHeymans, Stephane$$b38
000164129 7001_ $$aLyon, Alexander R$$b39
000164129 7001_ $$aBacks, Johannes$$b40
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