Cardiovascular disease and cancer: Evidence for shared disease pathways and pharmacologic prevention

Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are global priorities and major focus of World Health Organization's joint prevention programs. Emerging evidence suggests that modifiable risk f...

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Bibliographic Details
Published inAtherosclerosis Vol. 263; pp. 343 - 351
Main Authors Masoudkabir, Farzad, Sarrafzadegan, Nizal, Gotay, Carolyn, Ignaszewski, Andrew, Krahn, Andrew D., Davis, Margot K., Franco, Christopher, Mani, Arya
Format Journal Article
LanguageEnglish
Published Ireland Elsevier B.V 01.08.2017
Subjects
Animals
Anticarcinogenic Agents - therapeutic use
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Cardiovascular
Cardiovascular Agents - therapeutic use
Cardiovascular Diseases - genetics
Cardiovascular Diseases - metabolism
Cardiovascular Diseases - pathology
Cardiovascular Diseases - prevention & control
Cardiovascular System - drug effects
Cardiovascular System - metabolism
Cardiovascular System - pathology
Cell Transformation, Neoplastic - drug effects
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
Gene Expression Regulation, Neoplastic
Humans
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Neoplasms - prevention & control
Risk Factors
Signal Transduction - drug effects
CVD
T2DM
TZDs
CAD
RAAS
AMPK
PAI-1
VSMC
ACEIs/ARBs
PPAR-γ
WHO
Signaling pathways
Malignancy
Atherosclerosis
Online AccessGet full text
ISSN0021-9150
1879-1484
1879-1484
DOI10.1016/j.atherosclerosis.2017.06.001

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Abstract Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are global priorities and major focus of World Health Organization's joint prevention programs. Emerging evidence suggests that modifiable risk factors including diet, sedentary lifestyle, obesity and tobacco use are central to the pathogenesis of both diseases and are reflected in common genetic, cellular, and signaling mechanisms. Understanding this important biological overlap is critical and may help identify novel therapeutic and preventative strategies for both disorders. In this review, we will discuss the shared genetic and molecular factors central to CVD and cancer and how the strategies commonly used for the prevention of atherosclerotic vascular disease can be applied to cancer prevention. [Display omitted] •Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide.•CVD and cancer have common risk factors and shared genetics and molecular mechanisms that are central to their pathogenesis.•The shared pathways of CVD and cancer are potential targets for development of novel drugs for joint pharmacologic prevention of CVD and cancer.•A growing body of evidence supports a role for aspirin, statins, ACE inhibitors/ARBs, metformin, and TZDs in cancer prevention.•Both pharmacologic and non-pharmacologic preventive programs should be directed jointly at CVD and cancer.
AbstractList Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are global priorities and major focus of World Health Organization’s joint prevention programs. Emerging evidence suggests that modifiable risk factors including diet, sedentary lifestyle, obesity and tobacco use are central to the pathogenesis of both diseases and are reflected in common genetic, cellular, and signaling mechanisms. Understanding this important biological overlap is critical and may help identify novel therapeutic and preventative strategies for both disorders. In this review, we will discuss the shared genetic and molecular factors central to CVD and cancer and how the strategies commonly used for the prevention of atherosclerotic vascular disease can be applied to cancer prevention.
Abstract Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are global priorities and major focus of World Health Organization's joint prevention programs. Emerging evidence suggests that modifiable risk factors including diet, sedentary lifestyle, obesity and tobacco use are central to the pathogenesis of both diseases and are reflected in common genetic, cellular, and signaling mechanisms. Understanding this important biological overlap is critical and may help to identify novel therapeutic and preventative strategies for both disorders. In this review, we will discuss the shared genetic and molecular factors central to CVD and cancer and how the strategies commonly used for the prevention of atherosclerotic vascular disease can be applied to cancer prevention.
Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are global priorities and major focus of World Health Organization's joint prevention programs. Emerging evidence suggests that modifiable risk factors including diet, sedentary lifestyle, obesity and tobacco use are central to the pathogenesis of both diseases and are reflected in common genetic, cellular, and signaling mechanisms. Understanding this important biological overlap is critical and may help identify novel therapeutic and preventative strategies for both disorders. In this review, we will discuss the shared genetic and molecular factors central to CVD and cancer and how the strategies commonly used for the prevention of atherosclerotic vascular disease can be applied to cancer prevention.Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are global priorities and major focus of World Health Organization's joint prevention programs. Emerging evidence suggests that modifiable risk factors including diet, sedentary lifestyle, obesity and tobacco use are central to the pathogenesis of both diseases and are reflected in common genetic, cellular, and signaling mechanisms. Understanding this important biological overlap is critical and may help identify novel therapeutic and preventative strategies for both disorders. In this review, we will discuss the shared genetic and molecular factors central to CVD and cancer and how the strategies commonly used for the prevention of atherosclerotic vascular disease can be applied to cancer prevention.
Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are global priorities and major focus of World Health Organization's joint prevention programs. Emerging evidence suggests that modifiable risk factors including diet, sedentary lifestyle, obesity and tobacco use are central to the pathogenesis of both diseases and are reflected in common genetic, cellular, and signaling mechanisms. Understanding this important biological overlap is critical and may help identify novel therapeutic and preventative strategies for both disorders. In this review, we will discuss the shared genetic and molecular factors central to CVD and cancer and how the strategies commonly used for the prevention of atherosclerotic vascular disease can be applied to cancer prevention. [Display omitted] •Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide.•CVD and cancer have common risk factors and shared genetics and molecular mechanisms that are central to their pathogenesis.•The shared pathways of CVD and cancer are potential targets for development of novel drugs for joint pharmacologic prevention of CVD and cancer.•A growing body of evidence supports a role for aspirin, statins, ACE inhibitors/ARBs, metformin, and TZDs in cancer prevention.•Both pharmacologic and non-pharmacologic preventive programs should be directed jointly at CVD and cancer.
Author Mani, Arya
Masoudkabir, Farzad
Gotay, Carolyn
Franco, Christopher
Davis, Margot K.
Sarrafzadegan, Nizal
Ignaszewski, Andrew
Krahn, Andrew D.
AuthorAffiliation c School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada
d Cancer Control Research Program, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada
b Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
e Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada
f Yale Cardiovascular Genetics Program, Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA
a Cardiac Primary Prevention Research Center, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
AuthorAffiliation_xml – name: c School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada
– name: d Cancer Control Research Program, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada
– name: a Cardiac Primary Prevention Research Center, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
– name: e Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada
– name: b Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
– name: f Yale Cardiovascular Genetics Program, Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA
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  surname: Masoudkabir
  fullname: Masoudkabir, Farzad
  organization: Cardiac Primary Prevention Research Center, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
– sequence: 2
  givenname: Nizal
  surname: Sarrafzadegan
  fullname: Sarrafzadegan, Nizal
  email: nsarrafzadegan@gmail.com
  organization: Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
– sequence: 3
  givenname: Carolyn
  surname: Gotay
  fullname: Gotay, Carolyn
  organization: School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada
– sequence: 4
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  surname: Ignaszewski
  fullname: Ignaszewski, Andrew
  organization: Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada
– sequence: 5
  givenname: Andrew D.
  surname: Krahn
  fullname: Krahn, Andrew D.
  organization: Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada
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  surname: Davis
  fullname: Davis, Margot K.
  organization: Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada
– sequence: 7
  givenname: Christopher
  surname: Franco
  fullname: Franco, Christopher
  organization: Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada
– sequence: 8
  givenname: Arya
  surname: Mani
  fullname: Mani, Arya
  organization: Yale Cardiovascular Genetics Program, Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28624099$$D View this record in MEDLINE/PubMed
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Mon Jul 21 06:06:10 EDT 2025
Wed Oct 01 05:14:22 EDT 2025
Thu Apr 24 23:06:57 EDT 2025
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Tue Feb 25 19:57:36 EST 2025
Tue Aug 26 16:36:42 EDT 2025
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Keywords CVD
T2DM
TZDs
CAD
RAAS
AMPK
PAI-1
VSMC
ACEIs/ARBs
PPAR-γ
WHO
Signaling pathways
Malignancy
Atherosclerosis
Language English
License Copyright © 2017 Elsevier B.V. All rights reserved.
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content type line 23
FMK was responsible for writing the draft of the manuscript, creating the figure and tables and performing major revision of the manuscript. NS developed the idea, wrote some parts, edited the whole manuscript and supervised the whole project. CG edited the whole manuscript and wrote some parts. AI contributed in idea development and edited the manuscript. AK was responsible for editing the whole manuscript and writing some parts. MD wrote the cardio-oncology section. CF critically edited the whole manuscript and shortened the manuscript. AM was responsible for scientific support of the genetic and molecular pathways and did the major revisions.
Author contributions
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Snippet Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention are...
Abstract Cardiovascular disease (CVD) and cancer are leading causes of mortality and morbidity worldwide. Strategies to improve their treatment and prevention...
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SubjectTerms Animals
Anticarcinogenic Agents - therapeutic use
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Cardiovascular
Cardiovascular Agents - therapeutic use
Cardiovascular Diseases - genetics
Cardiovascular Diseases - metabolism
Cardiovascular Diseases - pathology
Cardiovascular Diseases - prevention & control
Cardiovascular System - drug effects
Cardiovascular System - metabolism
Cardiovascular System - pathology
Cell Transformation, Neoplastic - drug effects
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
Gene Expression Regulation, Neoplastic
Humans
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Neoplasms - prevention & control
Risk Factors
Signal Transduction - drug effects
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Title Cardiovascular disease and cancer: Evidence for shared disease pathways and pharmacologic prevention
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https://www.clinicalkey.es/playcontent/1-s2.0-S0021915017302484
https://dx.doi.org/10.1016/j.atherosclerosis.2017.06.001
https://www.ncbi.nlm.nih.gov/pubmed/28624099
https://www.proquest.com/docview/1911198889
https://pubmed.ncbi.nlm.nih.gov/PMC6207942
https://www.ncbi.nlm.nih.gov/pmc/articles/6207942
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