Skip to main content
Erschienen in: Current Oncology Reports 6/2016

01.06.2016 | Cardio-oncology (EH Yang, Section Editor)

Tyrosine Kinase Inhibitors and Vascular Toxicity: Impetus for a Classification System?

verfasst von: Joerg Herrmann

Erschienen in: Current Oncology Reports | Ausgabe 6/2016

Einloggen, um Zugang zu erhalten

Abstract

The introduction of molecularly targeted therapies with tyrosine kinase inhibitors has revolutionized cancer therapy and has contributed to a steady decline in cancer-related mortality since the late 1990s. However, not only cardiac but also vascular toxicity has been reported for these agents, some as expected on-target effects (e.g., VEGF receptor inhibitors) and others as unanticipated events (e.g., BCR-Abl inhibitors). A sound understanding of these cardiovascular toxic effects is critical to advance mechanistic insight into vascular disease and clinical care. From a conceptual standpoint, there might be value in defining type I (permanent) and type II (transient) vascular toxicity. This review will focus on the tyrosine kinase inhibitors in current clinical use and their associated vascular side effects.
Literatur
1.
Zurück zum Zitat Krause DS, Van Etten RA. Tyrosine kinases as targets for cancer therapy. N Engl J Med. 2005;353:172–87.CrossRefPubMed Krause DS, Van Etten RA. Tyrosine kinases as targets for cancer therapy. N Engl J Med. 2005;353:172–87.CrossRefPubMed
2.
Zurück zum Zitat Polk A, Vistisen K, Vaage-Nilsen M, Nielsen DL. A systematic review of the pathophysiology of 5-fluorouracil-induced cardiotoxicity. BMC Pharmacol Toxicol. 2014;15:47.CrossRefPubMedPubMedCentral Polk A, Vistisen K, Vaage-Nilsen M, Nielsen DL. A systematic review of the pathophysiology of 5-fluorouracil-induced cardiotoxicity. BMC Pharmacol Toxicol. 2014;15:47.CrossRefPubMedPubMedCentral
3.
Zurück zum Zitat Doll DC, List AF, Greco FA, Hainsworth JD, Hande KR, Johnson DH. Acute vascular ischemic events after cisplatin-based combination chemotherapy for germ-cell tumors of the testis. Ann Intern Med. 1986;105:48–51.CrossRefPubMed Doll DC, List AF, Greco FA, Hainsworth JD, Hande KR, Johnson DH. Acute vascular ischemic events after cisplatin-based combination chemotherapy for germ-cell tumors of the testis. Ann Intern Med. 1986;105:48–51.CrossRefPubMed
4.
Zurück zum Zitat Cortes JE, Kantarjian H, Shah NP, Bixby D, Mauro MJ, Flinn I, et al. Ponatinib in refractory Philadelphia chromosome-positive leukemias. N Engl J Med. 2012;367:2075–88.CrossRefPubMedPubMedCentral Cortes JE, Kantarjian H, Shah NP, Bixby D, Mauro MJ, Flinn I, et al. Ponatinib in refractory Philadelphia chromosome-positive leukemias. N Engl J Med. 2012;367:2075–88.CrossRefPubMedPubMedCentral
5.
Zurück zum Zitat Cortes JE, Kim DW, Pinilla-Ibarz J, le Coutre P, Paquette R, Chuah C, et al. A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias. N Engl J Med. 2013;369:1783–96.CrossRefPubMed Cortes JE, Kim DW, Pinilla-Ibarz J, le Coutre P, Paquette R, Chuah C, et al. A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias. N Engl J Med. 2013;369:1783–96.CrossRefPubMed
6.
Zurück zum Zitat Ewer MS, Lippman SM. Type II chemotherapy-related cardiac dysfunction: time to recognize a new entity. J Clin Oncol. 2005;23:2900–2.CrossRefPubMed Ewer MS, Lippman SM. Type II chemotherapy-related cardiac dysfunction: time to recognize a new entity. J Clin Oncol. 2005;23:2900–2.CrossRefPubMed
7.
Zurück zum Zitat Wu P, Nielsen TE, Clausen MH. FDA-approved small-molecule kinase inhibitors. Trends Pharmacol Sci. 2015;36:422–39.CrossRefPubMed Wu P, Nielsen TE, Clausen MH. FDA-approved small-molecule kinase inhibitors. Trends Pharmacol Sci. 2015;36:422–39.CrossRefPubMed
8.
Zurück zum Zitat Lassila M, Allen TJ, Cao Z, Thallas V, Jandeleit-Dahm KA, Candido R, et al. Imatinib attenuates diabetes-associated atherosclerosis. Arterioscler Thromb Vasc Biol. 2004;24:935–42.CrossRefPubMed Lassila M, Allen TJ, Cao Z, Thallas V, Jandeleit-Dahm KA, Candido R, et al. Imatinib attenuates diabetes-associated atherosclerosis. Arterioscler Thromb Vasc Biol. 2004;24:935–42.CrossRefPubMed
9.
Zurück zum Zitat Aman J, van Bezu J, Damanafshan A, Huveneers S, Eringa EC, Vogel SM, et al. Effective treatment of edema and endothelial barrier dysfunction with imatinib. Circulation. 2012;126:2728–38.CrossRefPubMed Aman J, van Bezu J, Damanafshan A, Huveneers S, Eringa EC, Vogel SM, et al. Effective treatment of edema and endothelial barrier dysfunction with imatinib. Circulation. 2012;126:2728–38.CrossRefPubMed
10.•
Zurück zum Zitat Chislock EM, Pendergast AM. Abl family kinases regulate endothelial barrier function in vitro and in mice. PLoS One. 2013;8, e85231. This study showed for the first time that endothelial Abl is directly involved in the regulation of vascular permeability, e.g. induced by vascular endothelial growth factor, in vitro and in vivo. Chislock EM, Pendergast AM. Abl family kinases regulate endothelial barrier function in vitro and in mice. PLoS One. 2013;8, e85231. This study showed for the first time that endothelial Abl is directly involved in the regulation of vascular permeability, e.g. induced by vascular endothelial growth factor, in vitro and in vivo.
11.
Zurück zum Zitat Montani D, Bergot E, Gunther S, Savale L, Bergeron A, Bourdin A, et al. Pulmonary arterial hypertension in patients treated by dasatinib. Circulation. 2012;125:2128–37.CrossRefPubMed Montani D, Bergot E, Gunther S, Savale L, Bergeron A, Bourdin A, et al. Pulmonary arterial hypertension in patients treated by dasatinib. Circulation. 2012;125:2128–37.CrossRefPubMed
12.
Zurück zum Zitat Jeon Y-W, Lee S-E, Kim S-H, Choi S-Y, Park J-E, Jeon H-R, et al. Six-year follow-up of dasatinib-related pulmonary arterial hypertension (PAH) for chronic myeloid leukemia in single center. Blood. 2013;122:4017. Jeon Y-W, Lee S-E, Kim S-H, Choi S-Y, Park J-E, Jeon H-R, et al. Six-year follow-up of dasatinib-related pulmonary arterial hypertension (PAH) for chronic myeloid leukemia in single center. Blood. 2013;122:4017.
13.
Zurück zum Zitat Shah NP, Wallis N, Farber HW, Mauro MJ, Wolf RA, Mattei D, et al. Clinical features of pulmonary arterial hypertension in patients receiving dasatinib. Am J Hematol. 2015;90:1060–4.CrossRefPubMed Shah NP, Wallis N, Farber HW, Mauro MJ, Wolf RA, Mattei D, et al. Clinical features of pulmonary arterial hypertension in patients receiving dasatinib. Am J Hematol. 2015;90:1060–4.CrossRefPubMed
14.•
Zurück zum Zitat Valent P, Hadzijusufovic E, Schernthaner GH, Wolf D, Rea D, le Coutre P. Vascular safety issues in CML patients treated with BCR/ABL1 kinase inhibitors. Blood. 2015;125:901–6. This review recapitulates the vascular toxicity aspects with the BCR/ABL1 kinase inhibitors nilotinib and ponatinib and provides recommendations for clinical practice. Valent P, Hadzijusufovic E, Schernthaner GH, Wolf D, Rea D, le Coutre P. Vascular safety issues in CML patients treated with BCR/ABL1 kinase inhibitors. Blood. 2015;125:901–6. This review recapitulates the vascular toxicity aspects with the BCR/ABL1 kinase inhibitors nilotinib and ponatinib and provides recommendations for clinical practice.
15.
Zurück zum Zitat de Lavallade H, Punnialingam S, Milojkovic D, Bua M, Khorashad JS, Gabriel IH, et al. Pleural effusions in patients with chronic myeloid leukaemia treated with dasatinib may have an immune-mediated pathogenesis. Br J Haematol. 2008;141:745–7.CrossRefPubMed de Lavallade H, Punnialingam S, Milojkovic D, Bua M, Khorashad JS, Gabriel IH, et al. Pleural effusions in patients with chronic myeloid leukaemia treated with dasatinib may have an immune-mediated pathogenesis. Br J Haematol. 2008;141:745–7.CrossRefPubMed
16.
Zurück zum Zitat Kim TD, Rea D, Schwarz M, Grille P, Nicolini FE, Rosti G, et al. Peripheral artery occlusive disease in chronic phase chronic myeloid leukemia patients treated with nilotinib or imatinib. Leukemia. 2013;27:1316–21.CrossRefPubMed Kim TD, Rea D, Schwarz M, Grille P, Nicolini FE, Rosti G, et al. Peripheral artery occlusive disease in chronic phase chronic myeloid leukemia patients treated with nilotinib or imatinib. Leukemia. 2013;27:1316–21.CrossRefPubMed
17.
Zurück zum Zitat Gijbels MJ, van der Cammen M, van der Laan LJ, Emeis JJ, Havekes LM, Hofker MH, et al. Progression and regression of atherosclerosis in APOE3-Leiden transgenic mice: an immunohistochemical study. Atherosclerosis. 1999;143:15–25.CrossRefPubMed Gijbels MJ, van der Cammen M, van der Laan LJ, Emeis JJ, Havekes LM, Hofker MH, et al. Progression and regression of atherosclerosis in APOE3-Leiden transgenic mice: an immunohistochemical study. Atherosclerosis. 1999;143:15–25.CrossRefPubMed
18.
Zurück zum Zitat Trogan E, Fayad ZA, Itskovich VV, Aguinaldo JG, Mani V, Fallon JT, et al. Serial studies of mouse atherosclerosis by in vivo magnetic resonance imaging detect lesion regression after correction of dyslipidemia. Arterioscler Thromb Vasc Biol. 2004;24:1714–9.CrossRefPubMed Trogan E, Fayad ZA, Itskovich VV, Aguinaldo JG, Mani V, Fallon JT, et al. Serial studies of mouse atherosclerosis by in vivo magnetic resonance imaging detect lesion regression after correction of dyslipidemia. Arterioscler Thromb Vasc Biol. 2004;24:1714–9.CrossRefPubMed
19.
Zurück zum Zitat Sattler KJ, Galili O, Rodriguez-Porcel M, Krier JD, Lerman LO, Lerman A. Dietary reversal of experimental hypercholesterolemia improves endothelial dysfunction of epicardial arteries but not of small coronary vessels in pigs. Atherosclerosis. 2006;188:301–8.CrossRefPubMed Sattler KJ, Galili O, Rodriguez-Porcel M, Krier JD, Lerman LO, Lerman A. Dietary reversal of experimental hypercholesterolemia improves endothelial dysfunction of epicardial arteries but not of small coronary vessels in pigs. Atherosclerosis. 2006;188:301–8.CrossRefPubMed
20.
Zurück zum Zitat Moslehi JJ, Deininger M. Tyrosine kinase inhibitor-associated cardiovascular toxicity in chronic myeloid leukemia. J Clin Oncol. 2015;33:4210–8.CrossRefPubMed Moslehi JJ, Deininger M. Tyrosine kinase inhibitor-associated cardiovascular toxicity in chronic myeloid leukemia. J Clin Oncol. 2015;33:4210–8.CrossRefPubMed
21.••
Zurück zum Zitat Chislock EM, Ring C, Pendergast AM. Abl kinases are required for vascular function, Tie2 expression, and angiopoietin-1-mediated survival. Proc Natl Acad Sci U S A. 2013;110:12432–7. The most important study to date on the significance of Abl kinases for endothelial cells, vascular development and function. Loss of endothelial Abl contributes to vascular dysfunction, infarction, and tissue damage. Central to these phenomena is the modulation of Tie2 expression and angiopoietin-1-mediated endothelial cell survival by endothelial Abl. Chislock EM, Ring C, Pendergast AM. Abl kinases are required for vascular function, Tie2 expression, and angiopoietin-1-mediated survival. Proc Natl Acad Sci U S A. 2013;110:12432–7. The most important study to date on the significance of Abl kinases for endothelial cells, vascular development and function. Loss of endothelial Abl contributes to vascular dysfunction, infarction, and tissue damage. Central to these phenomena is the modulation of Tie2 expression and angiopoietin-1-mediated endothelial cell survival by endothelial Abl.
22.
Zurück zum Zitat Hagensen MK, Raarup MK, Mortensen MB, Thim T, Nyengaard JR, Falk E, et al. Circulating endothelial progenitor cells do not contribute to regeneration of endothelium after murine arterial injury. Cardiovasc Res. 2012;93:223–31.CrossRefPubMed Hagensen MK, Raarup MK, Mortensen MB, Thim T, Nyengaard JR, Falk E, et al. Circulating endothelial progenitor cells do not contribute to regeneration of endothelium after murine arterial injury. Cardiovasc Res. 2012;93:223–31.CrossRefPubMed
23.
Zurück zum Zitat Hagensen MK, Shim J, Thim T, Falk E, Bentzon JF. Circulating endothelial progenitor cells do not contribute to plaque endothelium in murine atherosclerosis. Circulation. 2010;121:898–905.CrossRefPubMed Hagensen MK, Shim J, Thim T, Falk E, Bentzon JF. Circulating endothelial progenitor cells do not contribute to plaque endothelium in murine atherosclerosis. Circulation. 2010;121:898–905.CrossRefPubMed
24.
Zurück zum Zitat Loren CP, Aslan JE, Rigg RA, Nowak MS, Healy LD, Gruber A, et al. The BCR-ABL inhibitor ponatinib inhibits platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling, platelet activation and aggregate formation under shear. Thromb Res. 2015;135:155–60.CrossRefPubMedPubMedCentral Loren CP, Aslan JE, Rigg RA, Nowak MS, Healy LD, Gruber A, et al. The BCR-ABL inhibitor ponatinib inhibits platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling, platelet activation and aggregate formation under shear. Thromb Res. 2015;135:155–60.CrossRefPubMedPubMedCentral
25.
Zurück zum Zitat Herrmann J, Bell MR, Warren RL, Lerman A, Fleming MD, Patnaik M. Complicated and advanced atherosclerosis in a young woman with Philadelphia chromosome-positive acute lymphoblastic leukemia: success and challenges of BCR/ABL1-targeted cancer therapy. Mayo Clin Proc. 2015;90:1167–8.CrossRefPubMed Herrmann J, Bell MR, Warren RL, Lerman A, Fleming MD, Patnaik M. Complicated and advanced atherosclerosis in a young woman with Philadelphia chromosome-positive acute lymphoblastic leukemia: success and challenges of BCR/ABL1-targeted cancer therapy. Mayo Clin Proc. 2015;90:1167–8.CrossRefPubMed
26.
Zurück zum Zitat Breccia M, Colafigli G, Molica M, Alimena G. Cardiovascular risk assessments in chronic myeloid leukemia allow identification of patients at high risk of cardiovascular events during treatment with nilotinib. Am J Hematol. 2015;90:E100–1.CrossRefPubMed Breccia M, Colafigli G, Molica M, Alimena G. Cardiovascular risk assessments in chronic myeloid leukemia allow identification of patients at high risk of cardiovascular events during treatment with nilotinib. Am J Hematol. 2015;90:E100–1.CrossRefPubMed
27.••
Zurück zum Zitat Iliescu CA, Grines CL, Herrmann J, Yang EH, Cilingiroglu M, Charitakis K, et al. SCAI Expert consensus statement: evaluation, management, and special considerations of cardio-oncology patients in the cardiac catheterization laboratory (endorsed by the Cardiological Society of India, and Sociedad Latino Americana de Cardiologia Intervencionista). Catheter Cardiovasc Interv. 2016. doi:10.1002/ccd.26379. Highly important consensus statement as first of its kind directed primarily towards the care of cancer patients with vascular disease, including vascular disease induced by cancer therapies. Iliescu CA, Grines CL, Herrmann J, Yang EH, Cilingiroglu M, Charitakis K, et al. SCAI Expert consensus statement: evaluation, management, and special considerations of cardio-oncology patients in the cardiac catheterization laboratory (endorsed by the Cardiological Society of India, and Sociedad Latino Americana de Cardiologia Intervencionista). Catheter Cardiovasc Interv. 2016. doi:10.​1002/​ccd.​26379. Highly important consensus statement as first of its kind directed primarily towards the care of cancer patients with vascular disease, including vascular disease induced by cancer therapies.
28.
Zurück zum Zitat Plana JC, Galderisi M, Barac A, Ewer MS, Ky B, Scherrer-Crosbie M, et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2014;27:911–39.CrossRefPubMed Plana JC, Galderisi M, Barac A, Ewer MS, Ky B, Scherrer-Crosbie M, et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2014;27:911–39.CrossRefPubMed
29.
Zurück zum Zitat Ranpura V, Hapani S, Chuang J, Wu S. Risk of cardiac ischemia and arterial thromboembolic events with the angiogenesis inhibitor bevacizumab in cancer patients: a meta-analysis of randomized controlled trials. Acta Oncol. 2010;49:287–97.CrossRefPubMed Ranpura V, Hapani S, Chuang J, Wu S. Risk of cardiac ischemia and arterial thromboembolic events with the angiogenesis inhibitor bevacizumab in cancer patients: a meta-analysis of randomized controlled trials. Acta Oncol. 2010;49:287–97.CrossRefPubMed
30.
Zurück zum Zitat Schutz FA, Je Y, Azzi GR, Nguyen PL, Choueiri TK. Bevacizumab increases the risk of arterial ischemia: a large study in cancer patients with a focus on different subgroup outcomes. Ann Oncol. 2011;22:1404–12.CrossRefPubMed Schutz FA, Je Y, Azzi GR, Nguyen PL, Choueiri TK. Bevacizumab increases the risk of arterial ischemia: a large study in cancer patients with a focus on different subgroup outcomes. Ann Oncol. 2011;22:1404–12.CrossRefPubMed
31.
Zurück zum Zitat Chen XL, Lei YH, Liu CF, Yang QF, Zuo PY, Liu CY, et al. Angiogenesis inhibitor bevacizumab increases the risk of ischemic heart disease associated with chemotherapy: a meta-analysis. PLoS One. 2013;8, e66721.CrossRefPubMedPubMedCentral Chen XL, Lei YH, Liu CF, Yang QF, Zuo PY, Liu CY, et al. Angiogenesis inhibitor bevacizumab increases the risk of ischemic heart disease associated with chemotherapy: a meta-analysis. PLoS One. 2013;8, e66721.CrossRefPubMedPubMedCentral
32.
Zurück zum Zitat Choueiri TK, Schutz FA, Je Y, Rosenberg JE, Bellmunt J. Risk of arterial thromboembolic events with sunitinib and sorafenib: a systematic review and meta-analysis of clinical trials. J Clin Oncol. 2010;28:2280–5.CrossRefPubMed Choueiri TK, Schutz FA, Je Y, Rosenberg JE, Bellmunt J. Risk of arterial thromboembolic events with sunitinib and sorafenib: a systematic review and meta-analysis of clinical trials. J Clin Oncol. 2010;28:2280–5.CrossRefPubMed
33.
Zurück zum Zitat Qi WX, Shen Z, Tang LN, Yao Y. Risk of arterial thromboembolic events with vascular endothelial growth factor receptor tyrosine kinase inhibitors: an up-to-date meta-analysis. Crit Rev Oncol Hematol. 2014;92:71–82.CrossRefPubMed Qi WX, Shen Z, Tang LN, Yao Y. Risk of arterial thromboembolic events with vascular endothelial growth factor receptor tyrosine kinase inhibitors: an up-to-date meta-analysis. Crit Rev Oncol Hematol. 2014;92:71–82.CrossRefPubMed
34.
Zurück zum Zitat Motzer RJ, Hutson TE, Cella D, Reeves J, Hawkins R, Guo J, et al. Pazopanib versus sunitinib in metastatic renal-cell carcinoma. N Engl J Med. 2013;369:722–31.CrossRefPubMed Motzer RJ, Hutson TE, Cella D, Reeves J, Hawkins R, Guo J, et al. Pazopanib versus sunitinib in metastatic renal-cell carcinoma. N Engl J Med. 2013;369:722–31.CrossRefPubMed
35.
Zurück zum Zitat Isenberg JS, Martin-Manso G, Maxhimer JB, Roberts DD. Regulation of nitric oxide signalling by thrombospondin 1: implications for anti-angiogenic therapies. Nat Rev Cancer. 2009;9:182–94.CrossRefPubMedPubMedCentral Isenberg JS, Martin-Manso G, Maxhimer JB, Roberts DD. Regulation of nitric oxide signalling by thrombospondin 1: implications for anti-angiogenic therapies. Nat Rev Cancer. 2009;9:182–94.CrossRefPubMedPubMedCentral
36.
Zurück zum Zitat Kappers MH, van Esch JH, Sluiter W, Sleijfer S, Danser AH, van den Meiracker AH. Hypertension induced by the tyrosine kinase inhibitor sunitinib is associated with increased circulating endothelin-1 levels. Hypertension. 2010;56:675–81.CrossRefPubMed Kappers MH, van Esch JH, Sluiter W, Sleijfer S, Danser AH, van den Meiracker AH. Hypertension induced by the tyrosine kinase inhibitor sunitinib is associated with increased circulating endothelin-1 levels. Hypertension. 2010;56:675–81.CrossRefPubMed
37.••
Zurück zum Zitat Winnik S, Lohmann C, Siciliani G, von Lukowicz T, Kuschnerus K, Kraenkel N, et al. Systemic VEGF inhibition accelerates experimental atherosclerosis and disrupts endothelial homeostasis—implications for cardiovascular safety. Int J Cardiol. 2013;168:2453–61. Highly important study on the impact of a pan-vascular endothelial growth factor receptor tyrosine kinase inhibitor on atherosclerosis. The key findings are a reduction in nitric oxide production and availability and progression of atherosclerotic plaques but not plaque vulnerability. Winnik S, Lohmann C, Siciliani G, von Lukowicz T, Kuschnerus K, Kraenkel N, et al. Systemic VEGF inhibition accelerates experimental atherosclerosis and disrupts endothelial homeostasis—implications for cardiovascular safety. Int J Cardiol. 2013;168:2453–61. Highly important study on the impact of a pan-vascular endothelial growth factor receptor tyrosine kinase inhibitor on atherosclerosis. The key findings are a reduction in nitric oxide production and availability and progression of atherosclerotic plaques but not plaque vulnerability.
38.
Zurück zum Zitat Kappers MH, Smedts FM, Horn T, van Esch JH, Sleijfer S, Leijten F, et al. The vascular endothelial growth factor receptor inhibitor sunitinib causes a preeclampsia-like syndrome with activation of the endothelin system. Hypertension. 2011;58:295–302.CrossRefPubMed Kappers MH, Smedts FM, Horn T, van Esch JH, Sleijfer S, Leijten F, et al. The vascular endothelial growth factor receptor inhibitor sunitinib causes a preeclampsia-like syndrome with activation of the endothelin system. Hypertension. 2011;58:295–302.CrossRefPubMed
39.
Zurück zum Zitat Kappers MH, de Beer VJ, Zhou Z, Danser AH, Sleijfer S, Duncker DJ, et al. Sunitinib-induced systemic vasoconstriction in swine is endothelin mediated and does not involve nitric oxide or oxidative stress. Hypertension. 2012;59:151–7.CrossRefPubMed Kappers MH, de Beer VJ, Zhou Z, Danser AH, Sleijfer S, Duncker DJ, et al. Sunitinib-induced systemic vasoconstriction in swine is endothelin mediated and does not involve nitric oxide or oxidative stress. Hypertension. 2012;59:151–7.CrossRefPubMed
40.
Zurück zum Zitat Arima Y, Oshima S, Noda K, Fukushima H, Taniguchi I, Nakamura S, et al. Sorafenib-induced acute myocardial infarction due to coronary artery spasm. J Cardiol. 2009;54:512–5.CrossRefPubMed Arima Y, Oshima S, Noda K, Fukushima H, Taniguchi I, Nakamura S, et al. Sorafenib-induced acute myocardial infarction due to coronary artery spasm. J Cardiol. 2009;54:512–5.CrossRefPubMed
41.
Zurück zum Zitat Porto I, Leo A, Miele L, Pompili M, Landolfi R, Crea F. A case of variant angina in a patient under chronic treatment with sorafenib. Nat Rev Clin Oncol. 2010;7:476–80.CrossRefPubMed Porto I, Leo A, Miele L, Pompili M, Landolfi R, Crea F. A case of variant angina in a patient under chronic treatment with sorafenib. Nat Rev Clin Oncol. 2010;7:476–80.CrossRefPubMed
42.
Zurück zum Zitat Naib T, Steingart RM, Chen CL. Sorafenib-associated multivessel coronary artery vasospasm. Herz. 2011;36:348–51.CrossRefPubMed Naib T, Steingart RM, Chen CL. Sorafenib-associated multivessel coronary artery vasospasm. Herz. 2011;36:348–51.CrossRefPubMed
43.
Zurück zum Zitat Sen F, Yildiz I, Basaran M, Ekenel M, Oz F, Kilic L, et al. Impaired coronary flow reserve in metastatic cancer patients treated with sunitinib. J BUON. 2013;18:775–81.PubMed Sen F, Yildiz I, Basaran M, Ekenel M, Oz F, Kilic L, et al. Impaired coronary flow reserve in metastatic cancer patients treated with sunitinib. J BUON. 2013;18:775–81.PubMed
44.••
Zurück zum Zitat Chintalgattu V, Rees ML, Culver JC, Goel A, Jiffar T, Zhang J, et al. Coronary microvascular pericytes are the cellular target of sunitinib malate-induced cardiotoxicity. Sci Transl Med. 2013;5:187ra69. Outstanding work that deciphered for the first time the mechanisms of sunitinib-induced cardiotoxicity, which relate to microvascular dysfunction. Central to these effects is the impairment in platelet-derived growth factor signaling and elimination of the microvascular pericyte population. These observations have far reaching implications not only for the explanation of side effects of tyrosine kinase inhibitors blocking these pathways but also the interaction of pericytes and endothelial cells of the coronary microcirculation and their link with cardiac function. Chintalgattu V, Rees ML, Culver JC, Goel A, Jiffar T, Zhang J, et al. Coronary microvascular pericytes are the cellular target of sunitinib malate-induced cardiotoxicity. Sci Transl Med. 2013;5:187ra69. Outstanding work that deciphered for the first time the mechanisms of sunitinib-induced cardiotoxicity, which relate to microvascular dysfunction. Central to these effects is the impairment in platelet-derived growth factor signaling and elimination of the microvascular pericyte population. These observations have far reaching implications not only for the explanation of side effects of tyrosine kinase inhibitors blocking these pathways but also the interaction of pericytes and endothelial cells of the coronary microcirculation and their link with cardiac function.
45.
Zurück zum Zitat Pantaleo MA, Mandrioli A, Saponara M, Nannini M, Erente G, Lolli C, et al. Development of coronary artery stenosis in a patient with metastatic renal cell carcinoma treated with sorafenib. BMC Cancer. 2012;12:231.CrossRefPubMedPubMedCentral Pantaleo MA, Mandrioli A, Saponara M, Nannini M, Erente G, Lolli C, et al. Development of coronary artery stenosis in a patient with metastatic renal cell carcinoma treated with sorafenib. BMC Cancer. 2012;12:231.CrossRefPubMedPubMedCentral
46.
Zurück zum Zitat Ropert S, Vignaux O, Mir O, Goldwasser F. VEGF pathway inhibition by anticancer agent sunitinib and susceptibility to atherosclerosis plaque disruption. Invest New Drugs. 2011;29:1497–9.CrossRefPubMed Ropert S, Vignaux O, Mir O, Goldwasser F. VEGF pathway inhibition by anticancer agent sunitinib and susceptibility to atherosclerosis plaque disruption. Invest New Drugs. 2011;29:1497–9.CrossRefPubMed
47.
Zurück zum Zitat Moulton KS, Heller E, Konerding MA, Flynn E, Palinski W, Folkman J. Angiogenesis inhibitors endostatin or TNP-470 reduce intimal neovascularization and plaque growth in apolipoprotein E-deficient mice. Circulation. 1999;99:1726–32.CrossRefPubMed Moulton KS, Heller E, Konerding MA, Flynn E, Palinski W, Folkman J. Angiogenesis inhibitors endostatin or TNP-470 reduce intimal neovascularization and plaque growth in apolipoprotein E-deficient mice. Circulation. 1999;99:1726–32.CrossRefPubMed
48.
Zurück zum Zitat Moulton KS, Vakili K, Zurakowski D, Soliman M, Butterfield C, Sylvin E, et al. Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis. Proc Natl Acad Sci U S A. 2003;100:4736–41.CrossRefPubMedPubMedCentral Moulton KS, Vakili K, Zurakowski D, Soliman M, Butterfield C, Sylvin E, et al. Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis. Proc Natl Acad Sci U S A. 2003;100:4736–41.CrossRefPubMedPubMedCentral
49.
Zurück zum Zitat Herrmann J, Lerman LO, Mukhopadhyay D, Napoli C, Lerman A. Angiogenesis in atherogenesis. Arterioscler Thromb Vasc Biol. 2006;26:1948–57.CrossRefPubMed Herrmann J, Lerman LO, Mukhopadhyay D, Napoli C, Lerman A. Angiogenesis in atherogenesis. Arterioscler Thromb Vasc Biol. 2006;26:1948–57.CrossRefPubMed
50.
Zurück zum Zitat Hu S, Tian J, Dong N, Sun Y, Han X, Cheng W, et al. Bevacizumab for plaque stabilization: evaluation of its effect on vasa vasorum, lipid pool, and atheroma volume by multimodality imaging techniques in an atherosclerotic rabbit model. Circulation. 2012;126, A17934. Hu S, Tian J, Dong N, Sun Y, Han X, Cheng W, et al. Bevacizumab for plaque stabilization: evaluation of its effect on vasa vasorum, lipid pool, and atheroma volume by multimodality imaging techniques in an atherosclerotic rabbit model. Circulation. 2012;126, A17934.
51.
Zurück zum Zitat Holm PW, Slart RH, Zeebregts CJ, Hillebrands JL, Tio RA. Atherosclerotic plaque development and instability: a dual role for VEGF. Ann Med. 2009;41:257–64.CrossRefPubMed Holm PW, Slart RH, Zeebregts CJ, Hillebrands JL, Tio RA. Atherosclerotic plaque development and instability: a dual role for VEGF. Ann Med. 2009;41:257–64.CrossRefPubMed
52.
Zurück zum Zitat Kus T, Aktas G, Sevinc A, Kalender ME, Camci C. Could erlotinib treatment lead to acute cardiovascular events in patients with lung adenocarcinoma after chemotherapy failure? Onco Targets Ther. 2015;8:1341–3.CrossRefPubMedPubMedCentral Kus T, Aktas G, Sevinc A, Kalender ME, Camci C. Could erlotinib treatment lead to acute cardiovascular events in patients with lung adenocarcinoma after chemotherapy failure? Onco Targets Ther. 2015;8:1341–3.CrossRefPubMedPubMedCentral
53.
Zurück zum Zitat Ma W, Xu M, Liu Y, Liu H, Huang J, Zhu Y, et al. Safety profile of combined therapy inhibiting EFGR and VEGF pathways in patients with advanced non-small-cell lung cancer: a meta-analysis of 15 phase II/III randomized trials. Int J Cancer. 2015;137:409–19.CrossRefPubMed Ma W, Xu M, Liu Y, Liu H, Huang J, Zhu Y, et al. Safety profile of combined therapy inhibiting EFGR and VEGF pathways in patients with advanced non-small-cell lung cancer: a meta-analysis of 15 phase II/III randomized trials. Int J Cancer. 2015;137:409–19.CrossRefPubMed
54.
Zurück zum Zitat Scheffel RS, Dora JM, Siqueira DR, Burttet LM, Cerski MR, Maia AL. Toxic cardiomyopathy leading to fatal acute cardiac failure related to vandetanib: a case report with histopathological analysis. Eur J Endocrinol. 2013;168:K51–4.CrossRefPubMed Scheffel RS, Dora JM, Siqueira DR, Burttet LM, Cerski MR, Maia AL. Toxic cardiomyopathy leading to fatal acute cardiac failure related to vandetanib: a case report with histopathological analysis. Eur J Endocrinol. 2013;168:K51–4.CrossRefPubMed
55.
Zurück zum Zitat Kloth JS, Pagani A, Verboom MC, Malovini A, Napolitano C, Kruit WH, et al. Incidence and relevance of QTc-interval prolongation caused by tyrosine kinase inhibitors. Br J Cancer. 2015;112:1011–6.CrossRefPubMedPubMedCentral Kloth JS, Pagani A, Verboom MC, Malovini A, Napolitano C, Kruit WH, et al. Incidence and relevance of QTc-interval prolongation caused by tyrosine kinase inhibitors. Br J Cancer. 2015;112:1011–6.CrossRefPubMedPubMedCentral
56.
Zurück zum Zitat Schreier B, Gekle M, Grossmann C. Role of epidermal growth factor receptor in vascular structure and function. Curr Opin Nephrol Hypertens. 2014;23:113–21.CrossRefPubMed Schreier B, Gekle M, Grossmann C. Role of epidermal growth factor receptor in vascular structure and function. Curr Opin Nephrol Hypertens. 2014;23:113–21.CrossRefPubMed
57.
Zurück zum Zitat Ewer MS, Suter TM, Lenihan DJ, Niculescu L, Breazna A, Demetri GD, et al. Cardiovascular events among 1090 cancer patients treated with sunitinib, interferon, or placebo: a comprehensive adjudicated database analysis demonstrating clinically meaningful reversibility of cardiac events. Eur J Cancer. 2014;50:2162–70.CrossRefPubMed Ewer MS, Suter TM, Lenihan DJ, Niculescu L, Breazna A, Demetri GD, et al. Cardiovascular events among 1090 cancer patients treated with sunitinib, interferon, or placebo: a comprehensive adjudicated database analysis demonstrating clinically meaningful reversibility of cardiac events. Eur J Cancer. 2014;50:2162–70.CrossRefPubMed
58.
Zurück zum Zitat Srikanthan A, Ethier JL, Ocana A, Seruga B, Krzyzanowska MK, Amir E. Cardiovascular toxicity of multi-tyrosine kinase inhibitors in advanced solid tumors: a population-based observational study. PLoS One. 2015;10, e0122735.CrossRefPubMedPubMedCentral Srikanthan A, Ethier JL, Ocana A, Seruga B, Krzyzanowska MK, Amir E. Cardiovascular toxicity of multi-tyrosine kinase inhibitors in advanced solid tumors: a population-based observational study. PLoS One. 2015;10, e0122735.CrossRefPubMedPubMedCentral
Metadaten
Titel
Tyrosine Kinase Inhibitors and Vascular Toxicity: Impetus for a Classification System?
verfasst von
Joerg Herrmann
Publikationsdatum
01.06.2016
Verlag
Springer US
Erschienen in
Current Oncology Reports / Ausgabe 6/2016
Print ISSN: 1523-3790
Elektronische ISSN: 1534-6269
DOI
https://doi.org/10.1007/s11912-016-0514-0

Weitere Artikel der Ausgabe 6/2016

Current Oncology Reports 6/2016 Zur Ausgabe

Cardio-oncology (EH Yang, Section Editor)

Exercise Training in Cancer Survivors

Melanoma (RJ Sullivan, Section Editor)

Cell Cycle Regulation and Melanoma

Adjuvante Immuntherapie verlängert Leben bei RCC

25.04.2024 Nierenkarzinom Nachrichten

Nun gibt es auch Resultate zum Gesamtüberleben: Eine adjuvante Pembrolizumab-Therapie konnte in einer Phase-3-Studie das Leben von Menschen mit Nierenzellkarzinom deutlich verlängern. Die Sterberate war im Vergleich zu Placebo um 38% geringer.

Alectinib verbessert krankheitsfreies Überleben bei ALK-positivem NSCLC

25.04.2024 NSCLC Nachrichten

Das Risiko für Rezidiv oder Tod von Patienten und Patientinnen mit reseziertem ALK-positivem NSCLC ist unter einer adjuvanten Therapie mit dem Tyrosinkinase-Inhibitor Alectinib signifikant geringer als unter platinbasierter Chemotherapie.

Bei Senioren mit Prostatakarzinom auf Anämie achten!

24.04.2024 DGIM 2024 Nachrichten

Patienten, die zur Behandlung ihres Prostatakarzinoms eine Androgendeprivationstherapie erhalten, entwickeln nicht selten eine Anämie. Wer ältere Patienten internistisch mitbetreut, sollte auf diese Nebenwirkung achten.

ICI-Therapie in der Schwangerschaft wird gut toleriert

Müssen sich Schwangere einer Krebstherapie unterziehen, rufen Immuncheckpointinhibitoren offenbar nicht mehr unerwünschte Wirkungen hervor als andere Mittel gegen Krebs.

Update Onkologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.