Clonal Hematopoiesis Confers Predisposition to Both Cardiovascular Disease and Cancer
Authors: Abraham Aviv
Journal: Annals of Internal Medicine (2019)

Letters5 March 2019Clonal Hematopoiesis Confers Predisposition to Both Cardiovascular Disease and CancerAbraham Aviv, MDAbraham Aviv, MDThe Center of Human Development and Aging, Rutgers, The State University of New Jersey, New Jersey Medical School, Newark, New Jersey (A.A.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/L18-0637 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:I read Ebert and Libby's commentary (1) with interest. Telomere length dynamics may offer insight into the puzzling connection between clonal hematopoiesis of indeterminate potential (CHIP) and hematologic cancer and cardiovascular disease. My colleagues and I (2) recently proposed a 2-stage clonal expansion model for carcinogenesis based on the premise that a series of driver mutational hits (first hit) at the stem cell level generates a clone with replicative advantage; this stage is telomere length independent. A series of additional mutational hits (second hit) transforms the expanding clone into cancer; this stage is telomere length–dependent, meaning that ...References1. Ebert BL, Libby P. Clonal hematopoiesis confers predisposition to both cardiovascular disease and cancer: a newly recognized link between two major killers. Ann Intern Med. 2018;169:116-7. [PMID: 29809241]. doi:10.7326/M18-0737 LinkGoogle Scholar2. Aviv A, Anderson JJ, Shay JW. Mutations, cancer and the telomere length paradox. Trends Cancer. 2017;3:253-8. [PMID: 28718437] doi:10.1016/j.trecan.2017.02.005 CrossrefMedlineGoogle Scholar3. Steenstrup T, Kark JD, Verhulst S, Thinggaard M, Hjelmborg JVB, Dalgård C, et al. Telomeres and the natural lifespan limit in humans. Aging (Albany NY). 2017;9:1130-42. [PMID: 28394764] doi:10.18632/aging.101216 CrossrefMedlineGoogle Scholar4. Benetos A, Kark JD, Toupance S, Verhulst S, Aviv A. Response by Benetos et al to letter regarding article, “Short leukocyte telomere length precedes clinical expression of atherosclerosis: the blood-and-muscle model” [Letter]. Circ Res. 2018;122:e73-4. [PMID: 29650636] doi:10.1161/CIRCRESAHA.118.312967 CrossrefMedlineGoogle Scholar5. Stone RC, Horvath K, Kark JD, Susser E, Tishkoff SA, Aviv A. Telomere length and the cancer-atherosclerosis trade-off. PLoS Genet. 2016;12:e1006144. [PMID: 27386863] doi:10.1371/journal.pgen.1006144 CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: The Center of Human Development and Aging, Rutgers, The State University of New Jersey, New Jersey Medical School, Newark, New Jersey (A.A.)Disclosures: The author has disclosed no conflicts of interest. The form can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=L18-0637. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoClonal Hematopoiesis Confers Predisposition to Both Cardiovascular Disease and Cancer: A Newly Recognized Link Between Two Major Killers Benjamin L. Ebert and Peter Libby Metrics Cited byThe origin of leukemia: Genetic alterations and inflammatory factors in the development of premalignant clonal hematopoiesis 5 March 2019Volume 170, Issue 5Page: 356KeywordsAgingAtherosclerosisCarcinogenesisCardiovascular diseasesCellsGenetic diseasesHematologic malignanciesHematopoiesisMutationStem cells ePublished: 5 March 2019 Issue Published: 5 March 2019 Copyright & PermissionsCopyright © 2019 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...