Author + information
- Received July 25, 2019
- Revision received March 3, 2020
- Accepted March 23, 2020
- Published online May 25, 2020.
- Vivek Narayan, MD, MSCEa,b,
- Elizabeth W. Thompson, BSc,
- Biniyam Demissei, MD, MSC, PhDd,
- Jennifer E. Ho, MDe,
- James L. Januzzi Jr., MDf and
- Bonnie Ky, MD, MSCEb,d,g,∗ (, )@PennMedicine@JJheart_doc@JenHoCardiology
- aDivision of Hematology/Medical Oncology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
- bAbramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
- cPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
- dDivision of Cardiology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
- eCardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- fCardiology Division, Massachusetts General Hospital, Harvard Medical School, Baim Institute for Clinical Research, Boston, Massachusetts
- gDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
- ↵∗Address for correspondence:
Dr. Bonnie Ky, University of Pennsylvania School of Medicine, Smilow Center for Translational Research, 3400 Civic Center Boulevard, 11-105, Philadelphia, Pennsylvania 19104.
• CVD and cancer share several common pathophysiological mechanisms for disease incidence and progression.
• Several circulating and genomic biomarkers are reflective of this fundamental biological overlap and shared mechanisms.
• Before such biomarkers can be utilized in practice, their clinical role in enhancing risk prediction, screening, and therapeutic monitoring of both CVD and cancer should be further defined.
Cardiovascular disease (CVD) and cancer are leading causes of morbidity and mortality worldwide. Although conventionally managed as separate disease processes, recent research has lent insight into compelling commonalities between CVD and cancer, including shared mechanisms for disease development and progression. In this review, the authors discuss several pathophysiological processes common to both CVD and cancer, such as inflammation, resistance to cell death, cellular proliferation, neurohormonal stress, angiogenesis, and genomic instability, in an effort to understand common mechanisms of both disease states. In particular, the authors highlight key circulating and genomic biomarkers associated with each of these processes, as well as their associations with risk and prognosis in both cancer and CVD. The purpose of this state-of-the-art review is to further our understanding of the potential mechanisms underlying cancer and CVD by contextualizing pathways and biomarkers common to both diseases.
Ms. Thompson is supported by the American Heart Association Student Scholarship in Cardiovascular Disease, the Perelman School of Medicine Center for Clinical Epidemiology and Biostatistics Summer Research Fellowship, and the Okun Family Cardiovascular Scholarship. Dr. Ho is supported in part by National Institutes of Health grants R01-HL134893 and R01-HL140224; has received research support from Gilead Sciences and Bayer; and has received research supplies from EcoNugenics, Inc. Dr. Januzzi is supported in part by the Hutter Family Professorship; is a trustee of the American College of Cardiology; has received grant support from Novartis Pharmaceuticals, Roche Diagnostics, Abbott, Singulex, and Prevencio; has received consulting income from Abbott, Janssen, Novartis, Pfizer, Merck, and Roche Diagnostics; and has participated in clinical endpoint committees/data safety monitoring boards for Abbott, AbbVie, Amgen, Boehringer Ingelheim, Janssen, and Takeda. Dr. Ky is supported by National Heart, Lung, and Blood Institute grants R01-HL118018 and R21-HL141802; has previously received research support from Roche Diagnostics, Inc.; and has served as a consultant for Bristol-Myers Squibb. Dr. Narayan has received research grant support from Pfizer, Bristol-Myers Squibb, GlaxoSmithKline, and Peloton Therapeutics; and has served as a consultant for AstraZeneca, Merck, and Exilixis. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Suma H. Konety, M.D., M.S., served as Guest Associate Editor for this paper.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC author instructions page.
- Received July 25, 2019.
- Revision received March 3, 2020.
- Accepted March 23, 2020.
- 2020 American College of Cardiology Foundation
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