@article{3103467,
    title = "Common mechanistic pathways in cancer and heart failure. A scientific roadmap on behalf of the Translational Research Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)",
    author = "de Boer, R.A. and Hulot, J.-S. and Tocchetti, C.G. and Aboumsallem, J.P. and Ameri, P. and Anker, S.D. and Bauersachs, J. and Bertero, E. and Coats, A.J.S. and Čelutkienė, J. and Chioncel, O. and Dodion, P. and Eschenhagen, T. and Farmakis, D. and Bayes-Genis, A. and Jäger, D. and Jankowska, E.A. and Kitsis, R.N. and Konety, S.H. and Larkin, J. and Lehmann, L. and Lenihan, D.J. and Maack, C. and Moslehi, J.J. and Müller, O.J. and Nowak-Sliwinska, P. and Piepoli, M.F. and Ponikowski, P. and Pudil, R. and Rainer, P.P. and Ruschitzka, F. and Sawyer, D. and Seferovic, P.M. and Suter, T. and Thum, T. and van der Meer, P. and Van Laake, L.W. and von Haehling, S. and Heymans, S. and Lyon, A.R. and Backs, J.",
    journal = "European Journal of Heart Failure",
    year = "2020",
    volume = "22",
    number = "12",
    pages = "2272-2289",
    publisher = "John Wiley and Sons Ltd",
    doi = "10.1002/ejhf.2029",
    keywords = "antineoplastic agent;  cardiovascular agent, angiogenesis;  Article;  cachexia;  cancer incidence;  clinical practice;  heart failure;  hematopoiesis;  human;  inflammation;  malignant neoplasm;  metabolic activation;  nonhuman;  pathophysiology;  patient safety;  phase 1 clinical trial (topic);  phase 2 clinical trial (topic);  phase 3 clinical trial (topic);  preclinical study;  priority journal;  radiocardiography;  stroma cell;  tumor growth;  tumor microenvironment;  comorbidity;  heart failure;  neoplasm;  risk factor, Comorbidity;  Heart Failure;  Humans;  Inflammation;  Neoplasms;  Risk Factors",
    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. Furthermore, genetic predisposition and clonal haematopoiesis are common drivers for both conditions and they hold great clinical relevance in the context of personalized medicine. Additionally, altered angiogenesis is a common hallmark for failing hearts and tumours 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 two 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. To this aim, pre-clinical 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 patients from all ages, and men and women, with proper adjudication of both cancer and cardiovascular endpoints, are essential to accurately study these two pathologies at the same time. © 2020 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology."
}