Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024;24(1):2-12.
doi: 10.2174/011871529X307253240530060107.

Thrombosis in Myeloid Malignancies: From CHIP to AML

Beatrice Borsellino  1 , Carlos Bravo-Perez  2   3 , Valeria Visconte  2 , Luca Guarnera  1   2
Affiliations
Review

Thrombosis in Myeloid Malignancies: From CHIP to AML

Beatrice Borsellino et al. Cardiovasc Hematol Disord Drug Targets. 2024.

Abstract

The development of myeloid malignancies is a multi-step process starting from pre-malignant stages. Large-scale studies on clonal hematopoiesis of indeterminate potential (CHIP) identified this condition as a risk factor for developing hematologic malignancies, in particular myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). In parallel, CHIP was found to confer an enhanced thrombotic risk, in particular for cardiovascular diseases. In a similar fashion, in recent years, alongside their life-threatening features, increasing attention has been drawn toward thrombotic complications in myeloid malignancies. Thus, the purpose of this review is to gather a growing body of evidence on incidence, pathogenesis and clinical impact of thrombosis in myeloid malignancies at every step of malignant progression, from CHIP to AML.

Keywords: Thrombosis; VEXAS syndrome; acute myeloid leukemia; acute promyelocytic leukemia.; clonal hemopoiesis of indeterminate potential; myelodysplastic syndromes.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

References

    1. Guarnera L,; Santinella E,; Galossi E,; Microenvironment in Acute Myeloid Leukemia: focus on senescence mechanisms, therapeutic interactions and future directions. Exp Hematol 2023,129,104118 - DOI - PubMed
    1. Bouligny I.M.; Maher K.R.; Grant S.; Mechanisms of myeloid leukemogenesis: Current perspectives and therapeutic objectives. Blood Rev 2023,57,100996 - DOI - PubMed
    1. Genovese G.; Kähler A.K.; Handsaker R.E.; Lindberg J.; Rose S.A.; Bakhoum S.F.; Chambert K.; Mick E.; Neale B.M.; Fromer M.; Purcell S.M.; Svantesson O.; Landén M.; Höglund M.; Lehmann S.; Gabriel S.B.; Moran J.L.; Lander E.S.; Sullivan P.F.; Sklar P.; Grönberg H.; Hultman C.M.; McCarroll S.A.; Clonal hematopoiesis and blood-cancer risk inferred from blood DNA sequence. N Engl J Med 2014,371(26),2477-2487 - DOI - PubMed
    1. Jaiswal S.; Natarajan P.; Silver A.J.; Gibson C.J.; Bick A.G.; Shvartz E.; McConkey M.; Gupta N.; Gabriel S.; Ardissino D.; Baber U.; Mehran R.; Fuster V.; Danesh J.; Frossard P.; Saleheen D.; Melander O.; Sukhova G.K.; Neuberg D.; Libby P.; Kathiresan S.; Ebert B.L.; Clonal hematopoiesis and risk of atherosclerotic cardiovascular disease. N Engl J Med 2017,377(2),111-121 - DOI - PubMed
    1. Voso M.T.; Falconi G.; Fabiani E.; What’s new in the pathogenesis and treatment of therapy-related myeloid neoplasms. Blood 2021,138(9),749-757 - DOI - PubMed

MeSH terms