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dc.contributor.authorde Boer, RA
dc.contributor.authorHulot, J-S
dc.contributor.authorTocchetti, CG
dc.contributor.authorAboumsallem, JP
dc.contributor.authorAmeri, P
dc.contributor.authorAnker, SD
dc.contributor.authorBauersachs, J
dc.contributor.authorBertero, E
dc.contributor.authorCoats, AJS
dc.contributor.authorČelutkienė, J
dc.contributor.authorChioncel, O
dc.contributor.authorDodion, P
dc.contributor.authorEschenhagen, T
dc.contributor.authorFarmakis, D
dc.contributor.authorBayes-Genis, A
dc.contributor.authorJäger, D
dc.contributor.authorJankowska, EA
dc.contributor.authorKitsis, RN
dc.contributor.authorKonety, SH
dc.contributor.authorLarkin, J
dc.contributor.authorLehmann, L
dc.contributor.authorLenihan, DJ
dc.contributor.authorMaack, C
dc.contributor.authorMoslehi, JJ
dc.contributor.authorMüller, OJ
dc.contributor.authorNowak-Sliwinska, P
dc.contributor.authorPiepoli, MF
dc.contributor.authorPonikowski, P
dc.contributor.authorPudil, R
dc.contributor.authorRainer, PP
dc.contributor.authorRuschitzka, F
dc.contributor.authorSawyer, D
dc.contributor.authorSeferovic, PM
dc.contributor.authorSuter, T
dc.contributor.authorThum, T
dc.contributor.authorvan der Meer, P
dc.contributor.authorVan Laake, LW
dc.contributor.authorvon Haehling, S
dc.contributor.authorHeymans, S
dc.contributor.authorLyon, AR
dc.contributor.authorBacks, J
dc.coverage.spatialEngland
dc.date.accessioned2022-08-22T11:04:33Z
dc.date.available2022-08-22T11:04:33Z
dc.date.issued2020-11-12
dc.identifier.citationEuropean Journal of Heart Failure, 2020, 22 (12), pp. 2272 - 2289en_US
dc.identifier.issn1388-9842
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/5290
dc.identifier.eissn1879-0844
dc.identifier.eissn1879-0844
dc.identifier.doi10.1002/ejhf.2029
dc.description.abstractThe 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.
dc.formatPrint-Electronic
dc.format.extent2272 - 2289
dc.languageeng
dc.language.isoengen_US
dc.publisherWILEYen_US
dc.relation.ispartofEuropean Journal of Heart Failure
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.subjectAngiogenesis
dc.subjectCancer
dc.subjectCardio-oncology
dc.subjectCardiotoxicity
dc.subjectClonal haematopoiesis
dc.subjectExtracellular matrix
dc.subjectHeart failure
dc.subjectInflammation
dc.subjectMetabolism
dc.subjectComorbidity
dc.subjectHeart Failure
dc.subjectHumans
dc.subjectInflammation
dc.subjectNeoplasms
dc.subjectRisk Factors
dc.titleCommon 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).en_US
dc.typeJournal Article
dcterms.dateAccepted2020-10-18
dc.date.updated2022-08-22T11:04:04Z
rioxxterms.versionVoRen_US
rioxxterms.versionofrecord10.1002/ejhf.2029en_US
rioxxterms.licenseref.startdate2020-11-12
rioxxterms.typeJournal Article/Reviewen_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/33094495
pubs.issue12
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Melanoma and Kidney Cancer
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Melanoma and Kidney Cancer/Melanoma and Kidney Cancer (hon.)
pubs.publication-statusPublished
pubs.volume22
dc.contributor.icrauthorLarkin, James
icr.provenanceDeposited by Mr Arek Surman on 2022-08-22. Deposit type is initial. No. of files: 1. Files: Common mechanistic pathways in cancer and heart failure. A scientific roadmap on behalf of the Translational Research Commit.pdf


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