152
Views
0
CrossRef citations to date
0
Altmetric
Original Articles

High sensitivity c-reactive protein and circulating biomarkers of endothelial dysfunction in patients with chronic myeloid leukemia receiving tyrosine kinase inhibitors

ORCID Icon, , , ORCID Icon, &
Pages 2008-2017 | Received 10 Jan 2023, Accepted 05 Jul 2023, Published online: 09 Aug 2023

References

  • Bower H, Bjorkholm M, Dickman PW, et al. Life expectancy of patients with chronic myeloid leukemia approaches the life expectancy of the general population. J Clin Oncol. 2016; 34(24):2851–2857. doi:10.1200/JCO.2015.66.2866
  • Sukegawa M, Wang X, Nishioka C, et al. The BCR/ABL tyrosine kinase inhibitor, nilotinib, stimulates expression of IL-1β in vascular endothelium in association with downregulation of miR-3p. Leuk Res. 2017;58:83–90. doi:10.1016/j.leukres.2017.05.005
  • Hochhaus A, Larson RA, Guilhot F, et al. Long-term outcomes of imatinib treatment for chronic myeloid leukemia. N Engl J Med. 2017;376(10):917–927. doi:10.1056/NEJMoa1609324
  • Li W, Croce K, Steensma DP, et al. Vascular and metabolic implications of novel targeted cancer therapies: focus on kinase inhibitors. J Am Coll Cardiol. 2015;66(10):1160–1178. doi:10.1016/j.jacc.2015.07.025
  • Le Coutre P, Rea D, Abruzzese E, et al. Severe peripheral arterial disease during nilotinib therapy. J Natl Cancer Inst. 2011;103(17):1347–1348. doi:10.1093/jnci/djr292
  • Kim TD, Le Coutre P, Schwarz M, et al. Clinical cardiac safety profile of nilotinib. haematologica. 2012;97(6):883–889. doi:10.3324/haematol.2011.058776
  • Chai-Adisaksopha C, Lam W, Hillis C. Major arterial events in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors: a meta-analysis. Leuk Lymphoma. 2016;57(6):1300–1310. doi:10.3109/10428194.2015.1091929
  • Moslehi JJ, Deininger M. Tyrosine kinase inhibitor–associated cardiovascular toxicity in chronic myeloid leukemia. J Clin Oncol. 2015;33(35):4210–4218. doi:10.1200/JCO.2015.62.4718
  • Louvet C, Szot GL, Lang J, et al. Tyrosine kinase inhibitors reverse type 1 diabetes in nonobese diabetic mice. Proc Natl Acad Sci U S A. 2008;105(48):18895–18900. doi:10.1073/pnas.0810246105
  • Veneri D, Franchini M, Bonora E. Imatinib and regression of type 2 diabetes. N Engl J Med. 2005;352(10):1049–1050. doi:10.1056/NEJM200503103521023
  • Giles F, Mauro M, Hong F, et al. Rates of peripheral arterial occlusive disease in patients with chronic myeloid leukemia in the chronic phase treated with imatinib, nilotinib, or non-tyrosine kinase therapy: a retrospective cohort analysis. Leukemia. 2013;27(6):1310–1315. doi:10.1038/leu.2013.69
  • Valent P, Hadzijusufovic E, Schernthaner G-H, et al. Vascular safety issues in CML patients treated with BCR/ABL1 kinase inhibitors. Blood. 2015;125(6):901–906. doi:10.1182/blood-2014-09-594432
  • Kim T, Rea D, Schwarz M, et al. Peripheral artery occlusive disease in chronic phase chronic myeloid leukemia patients treated with nilotinib or imatinib. Leukemia. 2013;27(6):1316–1321. doi:10.1038/leu.2013.70
  • Kantarjian HM, Kim D-W, Pinilla-Ibarz J, et al. 2014; Ponatinib (PON) in patients (pts) with Philadelphia chromosome-positive (Ph+) leukemias resistant or intolerant to dasatinib or nilotinib, or with the T315I mutation: longer-term follow up of the PACE trial. J Clin Oncol. 2014 32:15_suppl, 7081-7081
  • Montani D, Bergot E, Günther S, et al. Pulmonary arterial hypertension in patients treated by dasatinib. Circulation. 2012; 125(17):2128–2137. doi:10.1161/CIRCULATIONAHA.111.079921
  • Aghel N, Delgado DH, Lipton JH. Cardiovascular toxicities of BCR-ABL tyrosine kinase inhibitors in chronic myeloid leukemia: preventive strategies and cardiovascular surveillance. Vasc Health Risk Manag. 2017;13:293–303. doi:10.2147/VHRM.S108874
  • Breccia M, Pregno P, Spallarossa P, et al. Identification, prevention and management of cardiovascular risk in chronic myeloid leukaemia patients candidate to ponatinib: an expert opinion. Ann Hematol. 2017;96(4):549–558. doi:10.1007/s00277-016-2820-x
  • Baccarani M, Deininger MW, Rosti G, 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
  • Hadi HA, Carr CS, Suwaidi A. J. Endothelial dysfunction: cardiovascular risk factors, therapy, and outcome. Vasc Health Risk Manag. 2005;1(3):183.
  • Gopal S, Lu Q, Man JJ, et al. A phosphoproteomic signature in endothelial cells predicts vascular toxicity of tyrosine kinase inhibitors used in CML. Blood Adv. 2018;2(14):1680–1684. doi:10.1182/bloodadvances.2018020396
  • Hadzijusufovic E, Albrecht-Schgoer K, Huber K, et al. Nilotinib-induced vasculopathy: identification of vascular endothelial cells as a primary target site. Leukemia. 2017;31(11):2388–2397. doi:10.1038/leu.2017.245
  • D'Agostino RB, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care: the framingham heart study. Circulation. 2008;117(6):743–753. doi:10.1161/CIRCULATIONAHA.107.699579
  • Yusuf S, Hawken S, Ôunpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):937–952. doi:10.1016/S0140-6736(04)17018-9
  • Corlin L, Liu C, Lin H, et al. Proteomic signatures of lifestyle risk factors for cardiovascular disease: a cross-sectional analysis of the plasma proteome in the Framingham heart study. J Am Heart Assoc. 2021; Jan 510(1):e018020.
  • Siemes C, Visser LE, Coebergh JW, et al. C-reactive protein levels, variation in the C-reactive protein gene, and cancer risk: the Rotterdam study. J Clin Oncol. 2006; 24(33):5216–5222. doi:10.1200/JCO.2006.07.1381
  • Ching C, Gustafson D, Thavendiranathan P, et al. Cancer therapy-related cardiac dysfunction: is endothelial dysfunction at the heart of the matter? Clin Sci (Lond). 2021;135(12):1487–1503. doi:10.1042/CS20210059
  • Seals DR, Jablonski KL, Donato AJ. Aging and vascular endothelial function in humans. Clin Sci (Lond). 2011;120(9):357–375. doi:10.1042/CS20100476
  • Latifi Y, Moccetti F, Wu M, et al. Thrombotic microangiopathy as a cause of cardiovascular toxicity from the BCR-ABL1 tyrosine kinase inhibitor ponatinib. Blood. 2019;133(14):1597–1606. doi:10.1182/blood-2018-10-881557
  • Pearson GJ, Thanassoulis G, Anderson TJ, et al. 2021 Canadian cardiovascular society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in adults. Can J Cardiol. 2021; 37(8):1129–1150. doi:10.1016/j.cjca.2021.03.016
  • Shao Y, Saredy J, Yang WY, et al. Vascular endothelial cells and innate immunity. Arterioscler Thromb Vasc Biol. 2020;40(6):e138–e152. doi:10.1161/ATVBAHA.120.314330
  • Gustafson D, Fish JE, Lipton JH, et al. Mechanisms of cardiovascular toxicity of BCR-ABL1 tyrosine kinase inhibitors in chronic myelogenous leukemia. Curr Hematol Malig Rep. 2020;15(1):20–30. doi:10.1007/s11899-020-00560-x
  • Gover-Proaktor A, Granot G, Shapira S, et al. Ponatinib reduces viability, migration, and functionality of human endothelial cells. Leuk Lymphoma. 2017;58(6):1455–1467. doi:10.1080/10428194.2016.1239258
  • Sicuranza A, Ferrigno I, Abruzzese E, et al. Pro-Inflammatory and Pro-Oxidative changes during nilotinib treatment in CML patients: results of a prospective multicenter Front-Line TKIs study (KIARO study). Front Oncol. 2022;12:835563. doi:10.3389/fonc.2022.835563
  • Leong D, Aghel N, Hillis C, et al. Tyrosine kinase inhibitors in chronic myeloid leukaemia and emergent cardiovascular disease. Heart. 2021;107(8):667–673. doi:10.1136/heartjnl-2020-318251
  • Aghel N, Lipton JH, Atenafu EG, et al. Cardiovascular events after exposure to nilotinib in chronic myeloid leukemia: long-term follow-up. Clin Lymphoma Myeloma Leuk. 2017; 17(12):870–878.e1. doi:10.1016/j.clml.2017.07.006
  • Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002; 105(9):1135–1143. doi:10.1161/hc0902.104353
  • Agca R, Smulders Y, Nurmohamed M. Cardiovascular disease risk in immune-mediated inflammatory diseases: recommendations for clinical practice. Heart. 2022; 108(1):73–79. doi:10.1136/heartjnl-2019-316378
  • Ridker PM, Rifai N, Rose L, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med. 2002;347(20):1557–1565. doi:10.1056/NEJMoa021993
  • Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195–2207. doi:10.1056/NEJMoa0807646
  • Koene RJ, Prizment AE, Blaes A, et al. Shared risk factors in cardiovascular disease and cancer. Circulation. 2016;133(11):1104–1114. doi:10.1161/CIRCULATIONAHA.115.020406
  • Jaiswal S, Libby P. Clonal haematopoiesis: connecting ageing and inflammation in cardiovascular disease. Nat Rev Cardiol. 2020;17(3):137–144. doi:10.1038/s41569-019-0247-5
  • Manouchehri A, Kanu E, Mauro MJ, et al. Tyrosine kinase inhibitors in leukemia and cardiovascular events: from mechanism to patient care. Arterioscler Thromb Vasc Biol. 2020;40(2):301–308. doi:10.1161/ATVBAHA.119.313353
  • Collaboration ERF. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. The Lancet. 2010;375(9709):132–140.
  • Gimbrone MA, Jr, García-Cardeña G. Vascular endothelium, hemodynamics, and the pathobiology of atherosclerosis. Cardiovasc Pathol. 2013;22(1):9–15. doi:10.1016/j.carpath.2012.06.006
  • Sattar N, McCarey DW, Capell H, et al. Explaining how “high-grade” systemic inflammation accelerates vascular risk in rheumatoid arthritis. Circulation. 2003;108(24):2957–2963. doi:10.1161/01.CIR.0000099844.31524.05
  • Pouwer MG, Pieterman EJ, Verschuren L, et al. The BCR-ABL1 inhibitors imatinib and ponatinib decrease plasma cholesterol and atherosclerosis, and nilotinib and ponatinib activate coagulation in a translational mouse model. Front Cardiovasc Med. 2018;5:55. doi:10.3389/fcvm.2018.00055
  • Paez-Mayorga J, Chen AL, Kotla S, et al. Ponatinib activates an inflammatory response in endothelial cells via ERK5 SUMOylation. Front Cardiovasc Med. 2018;5:125. doi:10.3389/fcvm.2018.00125
  • Sharma A, Burridge PW, McKeithan WL, Serrano R, Shukla P, Sayed N, Churko JM, Kitani T, Wu H, Holmström A, Matsa E, Zhang Y, Kumar A, Fan AC, Del Álamo JC, Wu SM, Moslehi JJ, Mercola M, Wu JC. High-throughput screening of tyrosine kinase inhibitor cardiotoxicity with human induced pluripotent stem cells. Sci Transl Med. 2017 Feb 15;9(377):eaaf2584. doi:10.1126/scitranslmed.aaf2584. PMID: 28202772; PMCID: PMC5409837

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.