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Review
. 2015 Dec 4;1(1):5.
doi: 10.1186/s40959-015-0008-5.

Tyrosine kinase inhibitor associated vascular toxicity in chronic myeloid leukemia

Oren Pasvolsky  1   2 , Avi Leader  1   2 , Zaza Iakobishvili  3   2 , Yishay Wasserstrum  3   2 , Ran Kornowski  3   2 , Pia Raanani  4   5
Affiliations
Review

Tyrosine kinase inhibitor associated vascular toxicity in chronic myeloid leukemia

Oren Pasvolsky et al. Cardiooncology. .

Abstract

Tyrosine kinase inhibitors (TKIs) have revolutionized the management and outcomes of chronic myeloid leukemia (CML) patients. Improved disease control and prolonged life expectancy now mandate focus on improving TKIs' safety profile. Recently, vascular adverse events (VAEs) have emerged as a serious consequence of some of the newer TKIs. In this review, we describe the clinical spectrum of TKI-associated VAE, and examine the unique vascular safety profile of the main TKIs currently used in the treatment of CML: imatinib, nilotinib, dasatinib, bosutinib and ponatinib. The issue of TKI-related platelet dysfunction is discussed as well. We describe the contemporary research findings regarding the possible pathogenesis of the VAE. Finally, the different aspects of TKI-associated VAE management are addressed, including prevention methods, monitoring strategies and treatment options.

Keywords: Chronic myeloid leukemia; Nilotinib; Platelets; Ponatinib; Tyrosine kinase inhibitor; Vascular adverse events.

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Figures

Fig. 1
Fig. 1
Comparative potency of BCR-ABL1 inhibition and selected off-target activity of tyrosine kinase inhibitors (TKIs). The figure describes the relative potencies of the various TKIs for BCR-ABL inhibition, as well as selected off-target activity of the various TKIs. Arrow width indicates potency. See text for further discussion
See this image and copyright information in PMC

References

    1. O’Brien SG, Guilhot F, Larson RA, Gathmann I, Baccarani M, Cervantes F, et al. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med. 2003;348(11):994–1004. doi: 10.1056/NEJMoa022457. - DOI - PubMed
    1. Jabbour EJ, Cortes JE, Kantarjian HM. Tyrosine kinase inhibition: a therapeutic target for the management of chronic-phase chronic myeloid leukemia. Expert Rev Anticancer Ther. 2013;13(12):1433–1452. doi: 10.1586/14737140.2013.859074. - DOI - PMC - PubMed
    1. Baccarani M, Deininger MW, Rosti G, Hochhaus A, Soverini S, Apperley JF, et al. European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013. Blood. 2013;122(6):872–884. doi: 10.1182/blood-2013-05-501569. - DOI - PMC - PubMed
    1. An X, Tiwari AK, Sun Y, Ding PR, Ashby CR, Jr, Chen ZS. BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. Leuk Res. 2010;34(10):1255–1268. doi: 10.1016/j.leukres.2010.04.016. - DOI - PubMed
    1. Saglio G, Kim DW, Issaragrisil S, le Coutre P, Etienne G, Lobo C, et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med. 2010;362(24):2251–2259. doi: 10.1056/NEJMoa0912614. - DOI - PubMed

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