Skip to main content
Erschienen in: Current Treatment Options in Oncology 4/2024

19.02.2024

A Comprehensive Review of Cancer Drug–Induced Cardiotoxicity in Blood Cancer Patients: Current Perspectives and Therapeutic Strategies

verfasst von: Vincenzo Costanzo, PhD, Yashwant Kumar Ratre, PhD, Emanuela Andretta, PhD, Rakesh Acharya, M.sc Zoology, L. V. K. S. Bhaskar, PhD, Henu Kumar Verma, PhD

Erschienen in: Current Treatment Options in Oncology | Ausgabe 4/2024

Einloggen, um Zugang zu erhalten

Opinion statement

Cardiotoxicity has emerged as a serious outcome catalyzed by various therapeutic targets in the field of cancer treatment, which includes chemotherapy, radiation, and targeted therapies. The growing significance of cancer drug–induced cardiotoxicity (CDIC) and radiation-induced cardiotoxicity (CRIC) necessitates immediate attention. This article intricately unveils how cancer treatments cause cardiotoxicity, which is exacerbated by patient-specific risks. In particular, drugs like anthracyclines, alkylating agents, and tyrosine kinase inhibitors pose a risk, along with factors such as hypertension and diabetes. Mechanistic insights into oxidative stress and topoisomerase-II-B inhibition are crucial, while cardiac biomarkers show early damage. Timely intervention and prompt treatment, especially with specific agents like dexrazoxane and beta-blockers, are pivotal in the proactive management of CDIC.
Literatur
1.
Zurück zum Zitat Kumar D, et al. Automatic detection of white blood cancer from bone marrow microscopic images using convolutional neural networks. IEEE Access. 2020;8:142521–31.CrossRef Kumar D, et al. Automatic detection of white blood cancer from bone marrow microscopic images using convolutional neural networks. IEEE Access. 2020;8:142521–31.CrossRef
2.
Zurück zum Zitat • Advancing Cancer Therapy. Nature Cancer. 2021;2(3):245–6. This article mentioned detailed view of recent updated cancer treatment option.CrossRef • Advancing Cancer Therapy. Nature Cancer. 2021;2(3):245–6. This article mentioned detailed view of recent updated cancer treatment option.CrossRef
4.
5.
Zurück zum Zitat Curigliano G, et al. Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations. Ann Oncol. 2020;31(2):171–90.PubMedCrossRef Curigliano G, et al. Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations. Ann Oncol. 2020;31(2):171–90.PubMedCrossRef
6.
Zurück zum Zitat Yu AF, Jones LW. Breast cancer treatment-associated cardiovascular toxicity and effects of exercise countermeasures. Cardio-Oncology. 2016;2(1):1.PubMedPubMedCentralCrossRef Yu AF, Jones LW. Breast cancer treatment-associated cardiovascular toxicity and effects of exercise countermeasures. Cardio-Oncology. 2016;2(1):1.PubMedPubMedCentralCrossRef
7.
Zurück zum Zitat Ginzac A, et al. Treatment-induced cardiotoxicity in breast cancer: a review of the interest of practicing a physical activity. Oncology. 2019;96(5):223–34.PubMedCrossRef Ginzac A, et al. Treatment-induced cardiotoxicity in breast cancer: a review of the interest of practicing a physical activity. Oncology. 2019;96(5):223–34.PubMedCrossRef
8.
Zurück zum Zitat Albini A, et al. Cardiotoxicity of anticancer drugs: the need for cardio-oncology and cardio-oncological prevention. J Natl Cancer Inst. 2010;102(1):14–25.PubMedPubMedCentralCrossRef Albini A, et al. Cardiotoxicity of anticancer drugs: the need for cardio-oncology and cardio-oncological prevention. J Natl Cancer Inst. 2010;102(1):14–25.PubMedPubMedCentralCrossRef
9.
Zurück zum Zitat Blanco JG, et al. Anthracycline-related cardiomyopathy after childhood cancer: role of polymorphisms in carbonyl reductase genes—a report from the Children’s Oncology Group. J Clin Oncol. 2012;30(13):1415.PubMedCrossRef Blanco JG, et al. Anthracycline-related cardiomyopathy after childhood cancer: role of polymorphisms in carbonyl reductase genes—a report from the Children’s Oncology Group. J Clin Oncol. 2012;30(13):1415.PubMedCrossRef
10.
Zurück zum Zitat Pavo N, et al. Cardiovascular biomarkers in patients with cancer and their association with all-cause mortality. Heart. 2015;101(23):1874–80.PubMedCrossRef Pavo N, et al. Cardiovascular biomarkers in patients with cancer and their association with all-cause mortality. Heart. 2015;101(23):1874–80.PubMedCrossRef
11.
Zurück zum Zitat Lipshultz SE, et al. Female sex and higher drug dose as risk factors for late cardiotoxic effects of doxorubicin therapy for childhood cancer. N Engl J Med. 1995;332(26):1738–44.PubMedCrossRef Lipshultz SE, et al. Female sex and higher drug dose as risk factors for late cardiotoxic effects of doxorubicin therapy for childhood cancer. N Engl J Med. 1995;332(26):1738–44.PubMedCrossRef
12.
Zurück zum Zitat Krischer JP, et al. Clinical cardiotoxicity following anthracycline treatment for childhood cancer: the Pediatric Oncology Group experience. J Clin Oncol. 1997;15(4):1544–52.PubMedCrossRef Krischer JP, et al. Clinical cardiotoxicity following anthracycline treatment for childhood cancer: the Pediatric Oncology Group experience. J Clin Oncol. 1997;15(4):1544–52.PubMedCrossRef
13.
Zurück zum Zitat Ezaz G, et al. Risk prediction model for heart failure and cardiomyopathy after adjuvant trastuzumab therapy for breast cancer. J Am Heart Assoc. 2014;3(1):e000472.PubMedPubMedCentralCrossRef Ezaz G, et al. Risk prediction model for heart failure and cardiomyopathy after adjuvant trastuzumab therapy for breast cancer. J Am Heart Assoc. 2014;3(1):e000472.PubMedPubMedCentralCrossRef
14.
Zurück zum Zitat Herrmann J, et al. Evaluation and management of patients with heart disease and cancer: cardio-oncology. Mayo Clin Proc. 2014. Elsevier. Herrmann J, et al. Evaluation and management of patients with heart disease and cancer: cardio-oncology. Mayo Clin Proc. 2014. Elsevier.
15.
Zurück zum Zitat Fogarassy G, et al. Risk prediction model for long-term heart failure incidence after epirubicin chemotherapy for breast cancer–a real-world data-based, nationwide classification analysis. Int J Cardiol. 2019;285:47–52.PubMedCrossRef Fogarassy G, et al. Risk prediction model for long-term heart failure incidence after epirubicin chemotherapy for breast cancer–a real-world data-based, nationwide classification analysis. Int J Cardiol. 2019;285:47–52.PubMedCrossRef
16.
Zurück zum Zitat Curigliano G, et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO Clinical Practice Guidelines. Ann Oncol. 2012;23(Suppl 7):vii155-66.PubMedCrossRef Curigliano G, et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO Clinical Practice Guidelines. Ann Oncol. 2012;23(Suppl 7):vii155-66.PubMedCrossRef
17.
Zurück zum Zitat Florea AM, Büsselberg D. Cisplatin as an anti-tumor drug: cellular mechanisms of activity, drug resistance and induced side effects. Cancers (Basel). 2011;3(1):1351–71.PubMedCrossRef Florea AM, Büsselberg D. Cisplatin as an anti-tumor drug: cellular mechanisms of activity, drug resistance and induced side effects. Cancers (Basel). 2011;3(1):1351–71.PubMedCrossRef
18.
Zurück zum Zitat Finet JE, Tang WHW. Protecting the heart in cancer therapy. F1000Res. 2018;28(7). Finet JE, Tang WHW. Protecting the heart in cancer therapy. F1000Res. 2018;28(7).
19.
Zurück zum Zitat Didagelos M, et al. Bleomycin cardiotoxicity during chemotherapy for an ovarian germ cell tumor. Hippokratia. 2013;17(2):187–8.PubMedPubMedCentral Didagelos M, et al. Bleomycin cardiotoxicity during chemotherapy for an ovarian germ cell tumor. Hippokratia. 2013;17(2):187–8.PubMedPubMedCentral
20.
Zurück zum Zitat Rajkumar SV. Multiple myeloma: 2018 update on diagnosis, risk-stratification, and management. Am J Hematol. 2018;93(8):1091–110.CrossRef Rajkumar SV. Multiple myeloma: 2018 update on diagnosis, risk-stratification, and management. Am J Hematol. 2018;93(8):1091–110.CrossRef
21.
Zurück zum Zitat Battisti NML, et al. Long-term outcome with targeted therapy in advanced/metastatic HER2-positive breast cancer: The Royal Marsden experience. Breast Cancer Res Treat. 2019;178(2):401–8.PubMedCrossRef Battisti NML, et al. Long-term outcome with targeted therapy in advanced/metastatic HER2-positive breast cancer: The Royal Marsden experience. Breast Cancer Res Treat. 2019;178(2):401–8.PubMedCrossRef
22.
Zurück zum Zitat Moslehi JJ, Deininger M. Tyrosine kinase inhibitor-associated cardiovascular toxicity in chronic myeloid leukemia. J Clin Oncol. 2015;33(35):4210–8.PubMedPubMedCentralCrossRef Moslehi JJ, Deininger M. Tyrosine kinase inhibitor-associated cardiovascular toxicity in chronic myeloid leukemia. J Clin Oncol. 2015;33(35):4210–8.PubMedPubMedCentralCrossRef
23.
Zurück zum Zitat Shacham-Abulafia A, et al. Real-life experience with ponatinib in chronic myeloid leukemia: a multicenter observational study. Clin Lymphoma Myeloma Leuk. 2018;18(7):e295–301.PubMedCrossRef Shacham-Abulafia A, et al. Real-life experience with ponatinib in chronic myeloid leukemia: a multicenter observational study. Clin Lymphoma Myeloma Leuk. 2018;18(7):e295–301.PubMedCrossRef
24.
Zurück zum Zitat Procopio G, et al. Sorafenib versus observation following radical metastasectomy for clear-cell renal cell carcinoma: results from the phase 2 randomized open-label RESORT study. Eur Urol Oncol. 2019;2(6):699–707.PubMedCrossRef Procopio G, et al. Sorafenib versus observation following radical metastasectomy for clear-cell renal cell carcinoma: results from the phase 2 randomized open-label RESORT study. Eur Urol Oncol. 2019;2(6):699–707.PubMedCrossRef
25.
Zurück zum Zitat Khaled H, et al. A multicenter, phase II study of the RAF-kinase inhibitor sorafenib in patients with advanced renal cell carcinoma. Mol Clin Oncol. 2015;3(5):1099–102.PubMedPubMedCentralCrossRef Khaled H, et al. A multicenter, phase II study of the RAF-kinase inhibitor sorafenib in patients with advanced renal cell carcinoma. Mol Clin Oncol. 2015;3(5):1099–102.PubMedPubMedCentralCrossRef
26.
Zurück zum Zitat Lee JL, et al. RandomizEd phase II trial of Sunitinib four weeks on and two weeks off versus two weeks on and one week off in metastatic clear-cell type REnal cell carcinoma: RESTORE trial. Ann Oncol. 2015;26(11):2300–5.PubMedCrossRef Lee JL, et al. RandomizEd phase II trial of Sunitinib four weeks on and two weeks off versus two weeks on and one week off in metastatic clear-cell type REnal cell carcinoma: RESTORE trial. Ann Oncol. 2015;26(11):2300–5.PubMedCrossRef
27.
Zurück zum Zitat Fausto C, et al. Nilotinib 300 mg twice daily: an academic single-arm study of newly diagnosed chronic phase chronic myeloid leukemia patients. Haematologica. 2016;101(10):1200–7.CrossRef Fausto C, et al. Nilotinib 300 mg twice daily: an academic single-arm study of newly diagnosed chronic phase chronic myeloid leukemia patients. Haematologica. 2016;101(10):1200–7.CrossRef
28.
Zurück zum Zitat Ganatra S, et al. Ibrutinib-associated atrial fibrillation. JACC Clin Electrophysiol. 2018;4(12):1491–500.PubMedCrossRef Ganatra S, et al. Ibrutinib-associated atrial fibrillation. JACC Clin Electrophysiol. 2018;4(12):1491–500.PubMedCrossRef
29.
Zurück zum Zitat Grothey A, et al. Evolving role of regorafenib for the treatment of advanced cancers. Cancer Treat Rev. 2020;86(101993):20. Grothey A, et al. Evolving role of regorafenib for the treatment of advanced cancers. Cancer Treat Rev. 2020;86(101993):20.
30.
Zurück zum Zitat de Lavallade H, et al. Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis. J Clin Oncol. 2008;26(20):3358–63.PubMedCrossRef de Lavallade H, et al. Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis. J Clin Oncol. 2008;26(20):3358–63.PubMedCrossRef
31.
Zurück zum Zitat Olshen A, et al. Dynamics of chronic myeloid leukemia response to dasatinib, nilotinib, and high-dose imatinib. Haematologica. 2014;99(11):1701–9.PubMedPubMedCentralCrossRef Olshen A, et al. Dynamics of chronic myeloid leukemia response to dasatinib, nilotinib, and high-dose imatinib. Haematologica. 2014;99(11):1701–9.PubMedPubMedCentralCrossRef
32.
Zurück zum Zitat •• Kamaraju S, et al. Interactions between cardiology and oncology drugs in precision cardio-oncology. Clin Sci. 2021;135(11):1333–51. Mentioned about detailed interactions of cardiology and oncology drugs in precision medicine.CrossRef •• Kamaraju S, et al. Interactions between cardiology and oncology drugs in precision cardio-oncology. Clin Sci. 2021;135(11):1333–51. Mentioned about detailed interactions of cardiology and oncology drugs in precision medicine.CrossRef
33.
Zurück zum Zitat Xu B, et al. Pyrotinib plus capecitabine versus lapatinib plus capecitabine for the treatment of HER2-positive metastatic breast cancer (PHOEBE): a multicentre, open-label, randomised, controlled, phase 3 trial. Lancet Oncol. 2021;22(3):351–60.PubMedCrossRef Xu B, et al. Pyrotinib plus capecitabine versus lapatinib plus capecitabine for the treatment of HER2-positive metastatic breast cancer (PHOEBE): a multicentre, open-label, randomised, controlled, phase 3 trial. Lancet Oncol. 2021;22(3):351–60.PubMedCrossRef
34.
Zurück zum Zitat Hauschild A, et al. Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre, open-label, phase 3 randomised controlled trial. Lancet. 2012;380(9839):358–65.PubMedCrossRef Hauschild A, et al. Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre, open-label, phase 3 randomised controlled trial. Lancet. 2012;380(9839):358–65.PubMedCrossRef
35.
Zurück zum Zitat Hoffner B, Benchich K. Trametinib: a targeted therapy in metastatic melanoma. J Adv Pract Oncol. 2018;9(7):741–5.PubMedPubMedCentral Hoffner B, Benchich K. Trametinib: a targeted therapy in metastatic melanoma. J Adv Pract Oncol. 2018;9(7):741–5.PubMedPubMedCentral
37.
Zurück zum Zitat Valenzuela MM, Neidigh JW, Wall NR. Antimetabolite treatment for pancreatic cancer. Chemotherapy. 2014;3(3):2167–7700. Valenzuela MM, Neidigh JW, Wall NR. Antimetabolite treatment for pancreatic cancer. Chemotherapy. 2014;3(3):2167–7700.
38.
Zurück zum Zitat Sethy C, Kundu CN. 5-Fluorouracil (5-FU) resistance and the new strategy to enhance the sensitivity against cancer: implication of DNA repair inhibition. Biomed Pharmacother. 2021;137:111285.PubMedCrossRef Sethy C, Kundu CN. 5-Fluorouracil (5-FU) resistance and the new strategy to enhance the sensitivity against cancer: implication of DNA repair inhibition. Biomed Pharmacother. 2021;137:111285.PubMedCrossRef
39.
Zurück zum Zitat Isakoff SJ, et al. Bosutinib plus capecitabine for selected advanced solid tumours: results of a phase 1 dose-escalation study. Br J Cancer. 2014;111(11):2058–66.PubMedPubMedCentralCrossRef Isakoff SJ, et al. Bosutinib plus capecitabine for selected advanced solid tumours: results of a phase 1 dose-escalation study. Br J Cancer. 2014;111(11):2058–66.PubMedPubMedCentralCrossRef
41.
Zurück zum Zitat Stoicescu EA, et al. Docetaxel for breast cancer treatment-side effects on ocular surface, a systematic review. Processes. 2021;9(7):1086.CrossRef Stoicescu EA, et al. Docetaxel for breast cancer treatment-side effects on ocular surface, a systematic review. Processes. 2021;9(7):1086.CrossRef
43.
Zurück zum Zitat Amaya C, et al. Exposure to low intensity ultrasound removes paclitaxel cytotoxicity in breast and ovarian cancer cells. BMC Cancer. 2021;21(1):981.PubMedPubMedCentralCrossRef Amaya C, et al. Exposure to low intensity ultrasound removes paclitaxel cytotoxicity in breast and ovarian cancer cells. BMC Cancer. 2021;21(1):981.PubMedPubMedCentralCrossRef
44.
Zurück zum Zitat Dhyani P, et al. Anticancer potential of alkaloids: a key emphasis to colchicine, vinblastine, vincristine, vindesine, vinorelbine and vincamine. Cancer Cell Int. 2022;22(1):206.PubMedPubMedCentralCrossRef Dhyani P, et al. Anticancer potential of alkaloids: a key emphasis to colchicine, vinblastine, vincristine, vindesine, vinorelbine and vincamine. Cancer Cell Int. 2022;22(1):206.PubMedPubMedCentralCrossRef
45.
Zurück zum Zitat • Jayaweera SPE, et al. Carfilzomib: a promising proteasome inhibitor for the treatment of relapsed and refractory multiple myeloma. Front Oncol. 2021;11(740796). This article shows the importance of carfilzomib for the treatment of relapsed and refractory multiple myeloma patients. • Jayaweera SPE, et al. Carfilzomib: a promising proteasome inhibitor for the treatment of relapsed and refractory multiple myeloma. Front Oncol. 2021;11(740796). This article shows the importance of carfilzomib for the treatment of relapsed and refractory multiple myeloma patients.
46.
Zurück zum Zitat Reneau JC, et al. Cardiotoxicity risk with bortezomib versus lenalidomide for treatment of multiple myeloma: a propensity matched study of 1,790 patients. Am J Hematol. 2017;92(2):E15–7. Reneau JC, et al. Cardiotoxicity risk with bortezomib versus lenalidomide for treatment of multiple myeloma: a propensity matched study of 1,790 patients. Am J Hematol. 2017;92(2):E15–7.
47.
Zurück zum Zitat Jouni H, et al. Ixazomib cardiotoxicity: a possible class effect of proteasome inhibitors. Am J Hematol. 2017;92(2):220–1.PubMedCrossRef Jouni H, et al. Ixazomib cardiotoxicity: a possible class effect of proteasome inhibitors. Am J Hematol. 2017;92(2):220–1.PubMedCrossRef
48.
Zurück zum Zitat Stenehjem JS, et al. Cardiorespiratory fitness in long-term lymphoma survivors after high-dose chemotherapy with autologous stem cell transplantation. Br J Cancer. 2016;115(2):178–87.PubMedPubMedCentralCrossRef Stenehjem JS, et al. Cardiorespiratory fitness in long-term lymphoma survivors after high-dose chemotherapy with autologous stem cell transplantation. Br J Cancer. 2016;115(2):178–87.PubMedPubMedCentralCrossRef
49.
Zurück zum Zitat Russo F, et al. The effects of fluorouracil, epirubicin, and cyclophosphamide (FEC60) on the intestinal barrier function and gut peptides in breast cancer patients: an observational study. BMC Cancer. 2013;13(1):56.PubMedPubMedCentralCrossRef Russo F, et al. The effects of fluorouracil, epirubicin, and cyclophosphamide (FEC60) on the intestinal barrier function and gut peptides in breast cancer patients: an observational study. BMC Cancer. 2013;13(1):56.PubMedPubMedCentralCrossRef
50.
Zurück zum Zitat Saleem T, Kasi A. Daunorubicin. Aug 28. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024. Saleem T, Kasi A. Daunorubicin. Aug 28. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024.
51.
Zurück zum Zitat Madeddu C, et al. Pathophysiology of cardiotoxicity induced by nonanthracycline chemotherapy. J Cardiovasc Med. 2016;17(1):0000000000000376. Madeddu C, et al. Pathophysiology of cardiotoxicity induced by nonanthracycline chemotherapy. J Cardiovasc Med. 2016;17(1):0000000000000376.
52.
Zurück zum Zitat Neelapu SS, et al. Society for Immunotherapy of Cancer (SITC) clinical practice guideline on immunotherapy for the treatment of lymphoma. J Immunother Cancer. 2020;8(2):2020–001235.CrossRef Neelapu SS, et al. Society for Immunotherapy of Cancer (SITC) clinical practice guideline on immunotherapy for the treatment of lymphoma. J Immunother Cancer. 2020;8(2):2020–001235.CrossRef
53.
Zurück zum Zitat •• Wang H, et al. Breaking the bottleneck in anticancer drug development: Efficient Utilization of Synthetic Biology. Molecules. 2022;27(21):7480. Article is highly recommended due to its important role in anticancer drug development. •• Wang H, et al. Breaking the bottleneck in anticancer drug development: Efficient Utilization of Synthetic Biology. Molecules. 2022;27(21):7480. Article is highly recommended due to its important role in anticancer drug development.
54.
Zurück zum Zitat Hortobagyi GJD. Anthracyclines in the treatment of cancer. Drugs. 1997;54(4):1–7.PubMed Hortobagyi GJD. Anthracyclines in the treatment of cancer. Drugs. 1997;54(4):1–7.PubMed
55.
Zurück zum Zitat Bhutani M, et al. Randomized study comparing 4′-epi-doxorubicin (Epirubicin) versus doxorubicin as a part of induction treatment in adult acute lymphoblastic leukemia. Am J Hematol. 2002;71(4):241–7.PubMedCrossRef Bhutani M, et al. Randomized study comparing 4′-epi-doxorubicin (Epirubicin) versus doxorubicin as a part of induction treatment in adult acute lymphoblastic leukemia. Am J Hematol. 2002;71(4):241–7.PubMedCrossRef
56.
Zurück zum Zitat Megías-Vericat JE, et al. Daunorubicin and cytarabine for certain types of poor-prognosis acute myeloid leukemia: a systematic literature review. Expert Rev Clin Pharmacol. 2019;12(3):197–218.PubMedCrossRef Megías-Vericat JE, et al. Daunorubicin and cytarabine for certain types of poor-prognosis acute myeloid leukemia: a systematic literature review. Expert Rev Clin Pharmacol. 2019;12(3):197–218.PubMedCrossRef
57.
Zurück zum Zitat Abraham R, Basser RL, Green MD. A risk-benefit assessment of anthracycline antibiotics in antineoplastic therapy. Drug Safety. 1996;15(6):406–29.PubMedCrossRef Abraham R, Basser RL, Green MD. A risk-benefit assessment of anthracycline antibiotics in antineoplastic therapy. Drug Safety. 1996;15(6):406–29.PubMedCrossRef
59.
Zurück zum Zitat Von Hoff DD, et al. Risk factors for doxorubicin-induced congestive heart failure. Ann Intern Med. 1979;91(5):710–7.CrossRef Von Hoff DD, et al. Risk factors for doxorubicin-induced congestive heart failure. Ann Intern Med. 1979;91(5):710–7.CrossRef
60.
Zurück zum Zitat Alexander J, et al. Serial assessment of doxorubicin cardiotoxicity with quantitative radionuclide angiocardiography. N Engl J Med. 1979;300(6):278–83.PubMedCrossRef Alexander J, et al. Serial assessment of doxorubicin cardiotoxicity with quantitative radionuclide angiocardiography. N Engl J Med. 1979;300(6):278–83.PubMedCrossRef
62.
Zurück zum Zitat Di Meo S, et al. Role of ROS and RNS sources in physiological and pathological conditions. Oxid Med Cell Longev. 2016;2016:1245049.PubMedPubMedCentral Di Meo S, et al. Role of ROS and RNS sources in physiological and pathological conditions. Oxid Med Cell Longev. 2016;2016:1245049.PubMedPubMedCentral
63.
Zurück zum Zitat Vara D, Pula G. Reactive oxygen species: physiological roles in the regulation of vascular cells. Curr Mol Med. 2014;14(9):1103–25.PubMedCrossRef Vara D, Pula G. Reactive oxygen species: physiological roles in the regulation of vascular cells. Curr Mol Med. 2014;14(9):1103–25.PubMedCrossRef
64.
Zurück zum Zitat Mikhed Y, et al. Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair. Redox Biol. 2015;5:275–89.PubMedPubMedCentralCrossRef Mikhed Y, et al. Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair. Redox Biol. 2015;5:275–89.PubMedPubMedCentralCrossRef
65.
Zurück zum Zitat Salvatorelli E, Menna P, Minotti G. Managing anthracycline-induced cardiotoxicity: beginning with the end in mind. Futur Cardiol. 2015;11(4):363–6.CrossRef Salvatorelli E, Menna P, Minotti G. Managing anthracycline-induced cardiotoxicity: beginning with the end in mind. Futur Cardiol. 2015;11(4):363–6.CrossRef
66.
Zurück zum Zitat Mercurio V, et al. Models of heart failure based on the cardiotoxicity of anticancer drugs. J Card Fail. 2016;22(6):449–58.PubMedCrossRef Mercurio V, et al. Models of heart failure based on the cardiotoxicity of anticancer drugs. J Card Fail. 2016;22(6):449–58.PubMedCrossRef
67.
Zurück zum Zitat Minotti G, et al. Pharmacological foundations of cardio-oncology. J Pharmacol Exp Ther. 2010;334(1):2–8.PubMedCrossRef Minotti G, et al. Pharmacological foundations of cardio-oncology. J Pharmacol Exp Ther. 2010;334(1):2–8.PubMedCrossRef
68.
Zurück zum Zitat Liu Y-Y, et al. Bacillus Calmette-Guerin and TLR4 agonist prevent cardiovascular hypertrophy and fibrosis by regulating immune microenvironment. J Immunol. 2008;180(11):7349–57.PubMedCrossRef Liu Y-Y, et al. Bacillus Calmette-Guerin and TLR4 agonist prevent cardiovascular hypertrophy and fibrosis by regulating immune microenvironment. J Immunol. 2008;180(11):7349–57.PubMedCrossRef
69.
Zurück zum Zitat Vejpongsa P. ETH Yeh, and Therapeutics, Topoisomerase 2β: a promising molecular target for primary prevention of anthracycline-induced cardiotoxicity. Clin Pharmacol Ther. 2014;95(1):45–52.PubMedCrossRef Vejpongsa P. ETH Yeh, and Therapeutics, Topoisomerase 2β: a promising molecular target for primary prevention of anthracycline-induced cardiotoxicity. Clin Pharmacol Ther. 2014;95(1):45–52.PubMedCrossRef
70.
Zurück zum Zitat Porto A, et al. Smooth muscle cells in human atherosclerotic plaques secrete and proliferate in response to high mobility group box 1 protein. FASEB J. 2006;20(14):2565–6.PubMedCrossRef Porto A, et al. Smooth muscle cells in human atherosclerotic plaques secrete and proliferate in response to high mobility group box 1 protein. FASEB J. 2006;20(14):2565–6.PubMedCrossRef
71.
72.
Zurück zum Zitat Birks EJ, et al. Increased toll-like receptor 4 in the myocardium of patients requiring left ventricular assist devices. J Heart Lung Transplant. 2004;23(2):228–35.PubMedCrossRef Birks EJ, et al. Increased toll-like receptor 4 in the myocardium of patients requiring left ventricular assist devices. J Heart Lung Transplant. 2004;23(2):228–35.PubMedCrossRef
73.
Zurück zum Zitat Armenian SH, et al. Prevention and monitoring of cardiac dysfunction in survivors of adult cancers: American Society of Clinical Oncology Clinical Practice Guideline. J Clin Oncol. 2017;35(8):893–911.PubMedCrossRef Armenian SH, et al. Prevention and monitoring of cardiac dysfunction in survivors of adult cancers: American Society of Clinical Oncology Clinical Practice Guideline. J Clin Oncol. 2017;35(8):893–911.PubMedCrossRef
74.
Zurück zum Zitat Legha SS, et al. Reduction of doxorubicin cardiotoxicity by prolonged continuous intravenous infusion. Ann Intern Med. 1982;96(2):133–9.PubMedCrossRef Legha SS, et al. Reduction of doxorubicin cardiotoxicity by prolonged continuous intravenous infusion. Ann Intern Med. 1982;96(2):133–9.PubMedCrossRef
75.
Zurück zum Zitat Lipshultz SE, et al. Doxorubicin administration by continuous infusion is not cardioprotective: the Dana-Farber 91–01 Acute Lymphoblastic Leukemia protocol. J Clin Oncol. 2002;20(6):1677–82.PubMedCrossRef Lipshultz SE, et al. Doxorubicin administration by continuous infusion is not cardioprotective: the Dana-Farber 91–01 Acute Lymphoblastic Leukemia protocol. J Clin Oncol. 2002;20(6):1677–82.PubMedCrossRef
76.
Zurück zum Zitat Plana JC, 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;15(10):1063–93. Plana JC, 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;15(10):1063–93.
77.
Zurück zum Zitat Gershwin ME, Goetzl EJ, Steinberg AD. Cyclophosphamide: use in practice. Ann Intern Med. 1974;80(4):531–40.PubMedCrossRef Gershwin ME, Goetzl EJ, Steinberg AD. Cyclophosphamide: use in practice. Ann Intern Med. 1974;80(4):531–40.PubMedCrossRef
78.
Zurück zum Zitat Zhao J, et al. High dose cyclophosphamide for cytoreduction in patients with acute myeloid leukemia with hyperleukocytosis or leukostasis. Leuk Lymphoma. 2021;62(5):1195–202.PubMedCrossRef Zhao J, et al. High dose cyclophosphamide for cytoreduction in patients with acute myeloid leukemia with hyperleukocytosis or leukostasis. Leuk Lymphoma. 2021;62(5):1195–202.PubMedCrossRef
79.
Zurück zum Zitat Sullivan MP, Ramirez I. Curability of Burkitt’s lymphoma with high-dose cyclophosphamide-high-dose methotrexate therapy and intrathecal chemoprophylaxis. J Clin Oncol. 1985;3(5):627–36.PubMedCrossRef Sullivan MP, Ramirez I. Curability of Burkitt’s lymphoma with high-dose cyclophosphamide-high-dose methotrexate therapy and intrathecal chemoprophylaxis. J Clin Oncol. 1985;3(5):627–36.PubMedCrossRef
80.
Zurück zum Zitat Devita VT Jr, Serpick AA, Carbone PP. Combination chemotherapy in the treatment of advanced Hodgkin’s disease. Ann Intern Med. 1970;73(6):881–95.PubMedCrossRef Devita VT Jr, Serpick AA, Carbone PP. Combination chemotherapy in the treatment of advanced Hodgkin’s disease. Ann Intern Med. 1970;73(6):881–95.PubMedCrossRef
81.
Zurück zum Zitat Skarin AT, et al. Combination chemotherapy of advanced non-Hodgkin lymphoma with bleomycin, adriamycin, cyclophosphamide, vincristine, and prednisone (BACOP). Blood. 1977;49(5):759–70.PubMed Skarin AT, et al. Combination chemotherapy of advanced non-Hodgkin lymphoma with bleomycin, adriamycin, cyclophosphamide, vincristine, and prednisone (BACOP). Blood. 1977;49(5):759–70.PubMed
82.
83.
Zurück zum Zitat Livingston R, et al. Small-cell carcinoma of the lung: combined chemotherapy and radiation: a Southwest Oncology Group study. Ann Intern Med. 1978;88(2):194–9.PubMedCrossRef Livingston R, et al. Small-cell carcinoma of the lung: combined chemotherapy and radiation: a Southwest Oncology Group study. Ann Intern Med. 1978;88(2):194–9.PubMedCrossRef
84.
Zurück zum Zitat Eder JP, et al. High-dose combination alkylating agent chemotherapy with autologous bone marrow support for metastatic breast cancer. J Clin Oncol. 1986;4(11):1592–7.PubMedCrossRef Eder JP, et al. High-dose combination alkylating agent chemotherapy with autologous bone marrow support for metastatic breast cancer. J Clin Oncol. 1986;4(11):1592–7.PubMedCrossRef
85.
Zurück zum Zitat Gottdiener JS, et al. Cardiotoxicity associated with high-dose cyclophosphamide therapy. Arch Intern Med. 1981;141(6):758–63.PubMedCrossRef Gottdiener JS, et al. Cardiotoxicity associated with high-dose cyclophosphamide therapy. Arch Intern Med. 1981;141(6):758–63.PubMedCrossRef
86.
Zurück zum Zitat Dow E, Schulman H. E Agura, Cyclophosphamide cardiac injury mimicking acute myocardial infarction. Bone Marrow Transplant. 1993;12(2):169–72.PubMed Dow E, Schulman H. E Agura, Cyclophosphamide cardiac injury mimicking acute myocardial infarction. Bone Marrow Transplant. 1993;12(2):169–72.PubMed
87.
Zurück zum Zitat Goldberg MA, et al. Cyclophosphamide cardiotoxicity: an analysis of dosing as a risk factor. Blood. 1986;68(5):1114–8.PubMedCrossRef Goldberg MA, et al. Cyclophosphamide cardiotoxicity: an analysis of dosing as a risk factor. Blood. 1986;68(5):1114–8.PubMedCrossRef
88.
Zurück zum Zitat Steinherz LJ, et al. Cardiac changes with cyclophosphamide. Med Pediatr Oncol. 1981;9(5):417–22.PubMedCrossRef Steinherz LJ, et al. Cardiac changes with cyclophosphamide. Med Pediatr Oncol. 1981;9(5):417–22.PubMedCrossRef
89.
Zurück zum Zitat Buja LM, Ferrans VJ, Graw RG Jr. Cardiac pathologic findings in patients treated with bone marrow transplantation. Human Pathol. 1976;7(1):17–45.CrossRef Buja LM, Ferrans VJ, Graw RG Jr. Cardiac pathologic findings in patients treated with bone marrow transplantation. Human Pathol. 1976;7(1):17–45.CrossRef
90.
Zurück zum Zitat Arora A, Scholar EM. Role of tyrosine kinase inhibitors in cancer therapy. J Pharmacol Exp Ther. 2005;315(3):971–9.PubMedCrossRef Arora A, Scholar EM. Role of tyrosine kinase inhibitors in cancer therapy. J Pharmacol Exp Ther. 2005;315(3):971–9.PubMedCrossRef
92.
Zurück zum Zitat Cheng H, Force T. Molecular mechanisms of cardiovascular toxicity of targeted cancer therapeutics. Circ Res. 2010;106(1):21–34.PubMedCrossRef Cheng H, Force T. Molecular mechanisms of cardiovascular toxicity of targeted cancer therapeutics. Circ Res. 2010;106(1):21–34.PubMedCrossRef
93.
Zurück zum Zitat Krause DS, Van Etten RA. Tyrosine kinases as targets for cancer therapy. N Engl J Med. 2005;353(2):172–87.PubMedCrossRef Krause DS, Van Etten RA. Tyrosine kinases as targets for cancer therapy. N Engl J Med. 2005;353(2):172–87.PubMedCrossRef
94.
Zurück zum Zitat Osborn M, Hughes T. Managing imatinib resistance in chronic myeloid leukaemia. Curr Opin Hematol. 2010;17(2):97–103.PubMedCrossRef Osborn M, Hughes T. Managing imatinib resistance in chronic myeloid leukaemia. Curr Opin Hematol. 2010;17(2):97–103.PubMedCrossRef
95.
Zurück zum Zitat Cortes JE, et al. Bosutinib versus imatinib for newly diagnosed chronic myeloid leukemia: results from the randomized BFORE trial. J Clin Oncol. 2018;36(3):231–7.PubMedCrossRef Cortes JE, et al. Bosutinib versus imatinib for newly diagnosed chronic myeloid leukemia: results from the randomized BFORE trial. J Clin Oncol. 2018;36(3):231–7.PubMedCrossRef
96.
Zurück zum Zitat Hazarika M, et al. Tasigna for chronic and accelerated phase Philadelphia chromosome–positive chronic myelogenous leukemia resistant to or intolerant of imatinib. Clin Cancer Res. 2008;14(17):5325–31.PubMedCrossRef Hazarika M, et al. Tasigna for chronic and accelerated phase Philadelphia chromosome–positive chronic myelogenous leukemia resistant to or intolerant of imatinib. Clin Cancer Res. 2008;14(17):5325–31.PubMedCrossRef
97.
Zurück zum Zitat Lee W-S, Kim JM. Cardiotoxicity associated with tyrosine kinase-targeted anticancer therapy. Mol Cell Toxicol. 2018;14(3):247–54.CrossRef Lee W-S, Kim JM. Cardiotoxicity associated with tyrosine kinase-targeted anticancer therapy. Mol Cell Toxicol. 2018;14(3):247–54.CrossRef
99.
Zurück zum Zitat Montani D, et al. Pulmonary arterial hypertension in patients treated by dasatinib. Circulation. 2012;125(17):2128–37.PubMedCrossRef Montani D, et al. Pulmonary arterial hypertension in patients treated by dasatinib. Circulation. 2012;125(17):2128–37.PubMedCrossRef
100.
Zurück zum Zitat Fazakas C, et al. Rho-kinase inhibition ameliorates dasatinib-induced endothelial dysfunction and pulmonary hypertension. Front Physiol. 2018;9:537.PubMedPubMedCentralCrossRef Fazakas C, et al. Rho-kinase inhibition ameliorates dasatinib-induced endothelial dysfunction and pulmonary hypertension. Front Physiol. 2018;9:537.PubMedPubMedCentralCrossRef
101.
Zurück zum Zitat Weatherald J, et al. Long-term outcomes of dasatinib-induced pulmonary arterial hypertension: a population-based study. Eur Respir J. 2017;50(1):1700217.PubMedCrossRef Weatherald J, et al. Long-term outcomes of dasatinib-induced pulmonary arterial hypertension: a population-based study. Eur Respir J. 2017;50(1):1700217.PubMedCrossRef
102.
Zurück zum Zitat Alkhatib Y, et al. The role of tyrosine kinase inhibitor “Lapatinib” in pulmonary hypertension. Pulm Pharmacol Ther. 2016;37:81–4.PubMedCrossRef Alkhatib Y, et al. The role of tyrosine kinase inhibitor “Lapatinib” in pulmonary hypertension. Pulm Pharmacol Ther. 2016;37:81–4.PubMedCrossRef
103.
Zurück zum Zitat Quilot F-M, et al. Pulmonary hypertension associated with ponatinib therapy. Eur Respir J. 2016;47(2):676–9.PubMedCrossRef Quilot F-M, et al. Pulmonary hypertension associated with ponatinib therapy. Eur Respir J. 2016;47(2):676–9.PubMedCrossRef
104.
Zurück zum Zitat Zakrzewski D, et al. Elevation of pulmonary artery pressure as a complication of nilotinib therapy for chronic myeloid leukemia. Int J Hematol. 2012;96(1):132–5.PubMedCrossRef Zakrzewski D, et al. Elevation of pulmonary artery pressure as a complication of nilotinib therapy for chronic myeloid leukemia. Int J Hematol. 2012;96(1):132–5.PubMedCrossRef
105.
Zurück zum Zitat Mourad J-J, et al. Blood pressure rise following angiogenesis inhibition by bevacizumab. A crucial role for microcirculation. Ann Oncol. 2008;19(5):927–34.PubMedCrossRef Mourad J-J, et al. Blood pressure rise following angiogenesis inhibition by bevacizumab. A crucial role for microcirculation. Ann Oncol. 2008;19(5):927–34.PubMedCrossRef
106.
Zurück zum Zitat Veronese ML, et al. Mechanisms of hypertension associated with BAY 43–9006. J Clin Oncol. 2006;24(9):1363–9.PubMedCrossRef Veronese ML, et al. Mechanisms of hypertension associated with BAY 43–9006. J Clin Oncol. 2006;24(9):1363–9.PubMedCrossRef
107.
Zurück zum Zitat Escudier B, et al. Bevacizumab plus interferon alfa-2a for treatment of metastatic renal cell carcinoma: a randomised, double-blind phase III trial. Lancet. 2007;370(9605):2103–11.PubMedCrossRef Escudier B, et al. Bevacizumab plus interferon alfa-2a for treatment of metastatic renal cell carcinoma: a randomised, double-blind phase III trial. Lancet. 2007;370(9605):2103–11.PubMedCrossRef
108.
Zurück zum Zitat Motzer RJ, et al. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med. 2007;356(2):115–24.PubMedCrossRef Motzer RJ, et al. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med. 2007;356(2):115–24.PubMedCrossRef
109.
Zurück zum Zitat Kerkelä R, et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med. 2006;12(8):908–16.PubMedCrossRef Kerkelä R, et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med. 2006;12(8):908–16.PubMedCrossRef
110.
Zurück zum Zitat Cheng H, Force T. Why do kinase inhibitors cause cardiotoxicity and what can be done about it? Prog Cardiovasc Dis. 2010;53(2):114–20.PubMedCrossRef Cheng H, Force T. Why do kinase inhibitors cause cardiotoxicity and what can be done about it? Prog Cardiovasc Dis. 2010;53(2):114–20.PubMedCrossRef
111.
Zurück zum Zitat Kerkela R, et al. Sunitinib-induced cardiotoxicity is mediated by off-target inhibition of AMP-activated protein kinase. Clin Transl Sci. 2009;2(1):15–25.PubMedPubMedCentralCrossRef Kerkela R, et al. Sunitinib-induced cardiotoxicity is mediated by off-target inhibition of AMP-activated protein kinase. Clin Transl Sci. 2009;2(1):15–25.PubMedPubMedCentralCrossRef
112.
Zurück zum Zitat Zamorano JL, et al. 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: The Task Force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC). Eur Heart J. 2016;37(36):2768–801.PubMedCrossRef Zamorano JL, et al. 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: The Task Force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC). Eur Heart J. 2016;37(36):2768–801.PubMedCrossRef
113.
Zurück zum Zitat Kantarjian H, et al. Nilotinib in imatinib-resistant CML and Philadelphia chromosome–positive ALL. N Engl J Med. 2006;354(24):2542–51.PubMedCrossRef Kantarjian H, et al. Nilotinib in imatinib-resistant CML and Philadelphia chromosome–positive ALL. N Engl J Med. 2006;354(24):2542–51.PubMedCrossRef
114.
Zurück zum Zitat Ponte ML, Keller GA, Girolamo G. Mechanisms of drug induced QT interval prolongation. Curr Drug Saf. 2010;5(1):44–53.PubMedCrossRef Ponte ML, Keller GA, Girolamo G. Mechanisms of drug induced QT interval prolongation. Curr Drug Saf. 2010;5(1):44–53.PubMedCrossRef
115.
Zurück zum Zitat Barbey JT, Pezzullo JC, Soignet SL. Effect of arsenic trioxide on QT interval in patients with advanced malignancies. J Clin Oncol. 2003;21(19):3609–15.PubMedCrossRef Barbey JT, Pezzullo JC, Soignet SL. Effect of arsenic trioxide on QT interval in patients with advanced malignancies. J Clin Oncol. 2003;21(19):3609–15.PubMedCrossRef
116.
Zurück zum Zitat Lee C-S, Rattu MA, Kim SS. A review of a novel, Bruton’s tyrosine kinase inhibitor, ibrutinib. J Oncol Pharm Pract. 2016;22(1):92–104.PubMedCrossRef Lee C-S, Rattu MA, Kim SS. A review of a novel, Bruton’s tyrosine kinase inhibitor, ibrutinib. J Oncol Pharm Pract. 2016;22(1):92–104.PubMedCrossRef
117.
Zurück zum Zitat Giudice V, Vecchione C, Selleri CJL. Cardiotoxicity of novel targeted hematological therapies. Life (Basel). 2020;10(12):344.PubMed Giudice V, Vecchione C, Selleri CJL. Cardiotoxicity of novel targeted hematological therapies. Life (Basel). 2020;10(12):344.PubMed
118.
Zurück zum Zitat Burger JA, et al. Long-term efficacy and safety of first-line ibrutinib treatment for patients with CLL/SLL: 5 years of follow-up from the phase 3 RESONATE-2 study. Leukemia. 2020;34(3):787–98.PubMedCrossRef Burger JA, et al. Long-term efficacy and safety of first-line ibrutinib treatment for patients with CLL/SLL: 5 years of follow-up from the phase 3 RESONATE-2 study. Leukemia. 2020;34(3):787–98.PubMedCrossRef
119.
Zurück zum Zitat McMullen JR, et al. Ibrutinib increases the risk of atrial fibrillation, potentially through inhibition of cardiac PI3K-Akt signaling. Blood. 2014;124(25):3829–30.PubMedCrossRef McMullen JR, et al. Ibrutinib increases the risk of atrial fibrillation, potentially through inhibition of cardiac PI3K-Akt signaling. Blood. 2014;124(25):3829–30.PubMedCrossRef
120.
Zurück zum Zitat Fradley MG, et al. Rates and risk of atrial arrhythmias in patients treated with ibrutinib compared with cytotoxic chemotherapy. Am J Cardiol. 2019;124(4):539–44.PubMedCrossRef Fradley MG, et al. Rates and risk of atrial arrhythmias in patients treated with ibrutinib compared with cytotoxic chemotherapy. Am J Cardiol. 2019;124(4):539–44.PubMedCrossRef
121.
122.
Zurück zum Zitat McMullen JR, et al. Protective effects of exercise and phosphoinositide 3-kinase (p110α) signaling in dilated and hypertrophic cardiomyopathy. Proc Natl Acad Sci USA. 2007;104(2):612–7.PubMedPubMedCentralCrossRef McMullen JR, et al. Protective effects of exercise and phosphoinositide 3-kinase (p110α) signaling in dilated and hypertrophic cardiomyopathy. Proc Natl Acad Sci USA. 2007;104(2):612–7.PubMedPubMedCentralCrossRef
123.
Zurück zum Zitat Pretorius L, et al. Reduced phosphoinositide 3-kinase (p110α) activation increases the susceptibility to atrial fibrillation. Am J Pathol. 2009;175(3):998–1009.PubMedPubMedCentralCrossRef Pretorius L, et al. Reduced phosphoinositide 3-kinase (p110α) activation increases the susceptibility to atrial fibrillation. Am J Pathol. 2009;175(3):998–1009.PubMedPubMedCentralCrossRef
124.
Zurück zum Zitat • Sayegh N, et al. Cardiovascular toxicities associated with tyrosine kinase inhibitors. Curr Cardiol Rep. 2023;25(4):269–80. Important article mentioned about cardiovascular toxicities associated with TKI.PubMedPubMedCentralCrossRef • Sayegh N, et al. Cardiovascular toxicities associated with tyrosine kinase inhibitors. Curr Cardiol Rep. 2023;25(4):269–80. Important article mentioned about cardiovascular toxicities associated with TKI.PubMedPubMedCentralCrossRef
126.
Zurück zum Zitat Rutledge CA, et al. c-Src kinase inhibition reduces arrhythmia inducibility and connexin43 dysregulation after myocardial infarction. J Am Coll Cardiol. 2014;63(9):928–34.PubMedPubMedCentralCrossRef Rutledge CA, et al. c-Src kinase inhibition reduces arrhythmia inducibility and connexin43 dysregulation after myocardial infarction. J Am Coll Cardiol. 2014;63(9):928–34.PubMedPubMedCentralCrossRef
127.
128.
129.
Zurück zum Zitat Herman SE, et al. The Bruton tyrosine kinase (BTK) inhibitor acalabrutinib demonstrates potent on-target effects and efficacy in two mouse models of chronic lymphocytic leukemiaACP-196 displays clinical activity in mouse models of CLL. Clin Cancer Res. 2017;23(11):2831–41.PubMedCrossRef Herman SE, et al. The Bruton tyrosine kinase (BTK) inhibitor acalabrutinib demonstrates potent on-target effects and efficacy in two mouse models of chronic lymphocytic leukemiaACP-196 displays clinical activity in mouse models of CLL. Clin Cancer Res. 2017;23(11):2831–41.PubMedCrossRef
130.
Zurück zum Zitat Herman SE, et al. Modeling tumor–host interactions of chronic lymphocytic leukemia in xenografted mice to study tumor biology and evaluate targeted therapy. Leukemia. 2013;27(12):2311–21.PubMedPubMedCentralCrossRef Herman SE, et al. Modeling tumor–host interactions of chronic lymphocytic leukemia in xenografted mice to study tumor biology and evaluate targeted therapy. Leukemia. 2013;27(12):2311–21.PubMedPubMedCentralCrossRef
131.
Zurück zum Zitat Khan Y, O’Brien S. Acalabrutinib and its use in treatment of chronic lymphocytic leukemia. Future Oncol. 2019;15(6):579–89.PubMedCrossRef Khan Y, O’Brien S. Acalabrutinib and its use in treatment of chronic lymphocytic leukemia. Future Oncol. 2019;15(6):579–89.PubMedCrossRef
132.
Zurück zum Zitat • Byrd JC, et al. Acalabrutinib monotherapy in patients with relapsed/refractory chronic lymphocytic leukemia: updated phase 2 results. Blood. 2020;135(15):1204–13. The article mentioned about clinical trial of monotherapy in in patients with relapsed/refractory chronic lymphocytic leukemia.PubMedPubMedCentralCrossRef • Byrd JC, et al. Acalabrutinib monotherapy in patients with relapsed/refractory chronic lymphocytic leukemia: updated phase 2 results. Blood. 2020;135(15):1204–13. The article mentioned about clinical trial of monotherapy in in patients with relapsed/refractory chronic lymphocytic leukemia.PubMedPubMedCentralCrossRef
133.
Zurück zum Zitat Blackmon A, O’Brien S. An update on acalabrutinib to treat chronic lymphocytic leukemia. Drugs Today. 2021;57(7):417–31.CrossRef Blackmon A, O’Brien S. An update on acalabrutinib to treat chronic lymphocytic leukemia. Drugs Today. 2021;57(7):417–31.CrossRef
134.
Zurück zum Zitat Sharman JP, et al. Acalabrutinib with or without obinutuzumab versus chlorambucil and obinutuzumab for treatment-naive chronic lymphocytic leukaemia (ELEVATE-TN): a randomised, controlled, phase 3 trial. Lancet. 2020;395(10232):1278–91.PubMedPubMedCentralCrossRef Sharman JP, et al. Acalabrutinib with or without obinutuzumab versus chlorambucil and obinutuzumab for treatment-naive chronic lymphocytic leukaemia (ELEVATE-TN): a randomised, controlled, phase 3 trial. Lancet. 2020;395(10232):1278–91.PubMedPubMedCentralCrossRef
135.
Zurück zum Zitat Jin Y, et al. A comprehensive review of clinical cardiotoxicity incidence of FDA-approved small-molecule kinase inhibitors. Front Pharmacol. 2020;11:891.PubMedPubMedCentralCrossRef Jin Y, et al. A comprehensive review of clinical cardiotoxicity incidence of FDA-approved small-molecule kinase inhibitors. Front Pharmacol. 2020;11:891.PubMedPubMedCentralCrossRef
136.
Zurück zum Zitat Byrd JC, et al. Acalabrutinib versus ibrutinib in previously treated chronic lymphocytic leukemia: results of the first randomized phase III trial. J Clin Oncol. 2021;39(31):3441–52.PubMedPubMedCentralCrossRef Byrd JC, et al. Acalabrutinib versus ibrutinib in previously treated chronic lymphocytic leukemia: results of the first randomized phase III trial. J Clin Oncol. 2021;39(31):3441–52.PubMedPubMedCentralCrossRef
137.
Zurück zum Zitat Shadman M, et al. Zanubrutinib in patients with previously treated B-cell malignancies intolerant of previous Bruton tyrosine kinase inhibitors in the USA: a phase 2, open-label, single-arm study. Lancet Haematol. 2023;10(1):e35–45.PubMedCrossRef Shadman M, et al. Zanubrutinib in patients with previously treated B-cell malignancies intolerant of previous Bruton tyrosine kinase inhibitors in the USA: a phase 2, open-label, single-arm study. Lancet Haematol. 2023;10(1):e35–45.PubMedCrossRef
138.
139.
Zurück zum Zitat Darby SC, et al. Radiation-related heart disease: current knowledge and future prospects. 2010;76(3):656-665. Darby SC, et al. Radiation-related heart disease: current knowledge and future prospects. 2010;76(3):656-665.
140.
Zurück zum Zitat Curigliano G, et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO Clinical Practice Guidelines. Ann Oncol. 2012;23:vii155–66.PubMedCrossRef Curigliano G, et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO Clinical Practice Guidelines. Ann Oncol. 2012;23:vii155–66.PubMedCrossRef
141.
Zurück zum Zitat Hancock SL, Tucker MA, Hoppe RT. Factors affecting late mortality from heart disease after treatment of Hodgkin’s disease. JAMA. 1993;270(16):1949–55.PubMedCrossRef Hancock SL, Tucker MA, Hoppe RT. Factors affecting late mortality from heart disease after treatment of Hodgkin’s disease. JAMA. 1993;270(16):1949–55.PubMedCrossRef
142.
Zurück zum Zitat Carr ZA, et al. Coronary heart disease after radiotherapy for peptic ulcer disease. Int J Radiat Oncol Biol Phys. 2005;61(3):842–50.PubMedCrossRef Carr ZA, et al. Coronary heart disease after radiotherapy for peptic ulcer disease. Int J Radiat Oncol Biol Phys. 2005;61(3):842–50.PubMedCrossRef
143.
Zurück zum Zitat Kikuchi K, et al. Effects of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival. Lancet. 2005;366(9503):2087–106.CrossRef Kikuchi K, et al. Effects of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival. Lancet. 2005;366(9503):2087–106.CrossRef
144.
Zurück zum Zitat Tukenova M, et al. Role of cancer treatment in long-term overall and cardiovascular mortality after childhood cancer. J Clin Oncol. 2010;28(8):1308–15.PubMedCrossRef Tukenova M, et al. Role of cancer treatment in long-term overall and cardiovascular mortality after childhood cancer. J Clin Oncol. 2010;28(8):1308–15.PubMedCrossRef
145.
146.
Zurück zum Zitat Metzger ML, et al. Association between radiotherapy vs no radiotherapy based on early response to VAMP chemotherapy and survival among children with favorable-risk Hodgkin lymphoma. JAMA. 2012;307(24):2609–16.PubMedPubMedCentralCrossRef Metzger ML, et al. Association between radiotherapy vs no radiotherapy based on early response to VAMP chemotherapy and survival among children with favorable-risk Hodgkin lymphoma. JAMA. 2012;307(24):2609–16.PubMedPubMedCentralCrossRef
147.
Zurück zum Zitat Tebbi CK, et al. Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin’s disease. J Clin Oncol. 2007;25(5):493–500.PubMedCrossRef Tebbi CK, et al. Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin’s disease. J Clin Oncol. 2007;25(5):493–500.PubMedCrossRef
148.
149.
Zurück zum Zitat Galper SL, et al. Clinically significant cardiac disease in patients with Hodgkin lymphoma treated with mediastinal irradiation. Blood. 2011;117(2):412–8.PubMedCrossRef Galper SL, et al. Clinically significant cardiac disease in patients with Hodgkin lymphoma treated with mediastinal irradiation. Blood. 2011;117(2):412–8.PubMedCrossRef
150.
Zurück zum Zitat Aleman BM, et al. Late cardiotoxicity after treatment for Hodgkin lymphoma. Blood. 2007;109(5):1878–86.PubMedCrossRef Aleman BM, et al. Late cardiotoxicity after treatment for Hodgkin lymphoma. Blood. 2007;109(5):1878–86.PubMedCrossRef
151.
Zurück zum Zitat Hull MC, et al. Valvular dysfunction and carotid, subclavian, and coronary artery disease in survivors of Hodgkin lymphoma treated with radiation therapy. JAMA. 2003;290(21):2831–7.PubMedCrossRef Hull MC, et al. Valvular dysfunction and carotid, subclavian, and coronary artery disease in survivors of Hodgkin lymphoma treated with radiation therapy. JAMA. 2003;290(21):2831–7.PubMedCrossRef
152.
Zurück zum Zitat Koutroumpakis E, et al. Modern radiotherapy and risk of cardiotoxicity. Chemotherapy. 2020;65(3–4):65–76.PubMedCrossRef Koutroumpakis E, et al. Modern radiotherapy and risk of cardiotoxicity. Chemotherapy. 2020;65(3–4):65–76.PubMedCrossRef
153.
Zurück zum Zitat Ebrahimian T, et al. Chronic exposure to external low-dose gamma radiation induces an increase in anti-inflammatory and anti-oxidative parameters resulting in atherosclerotic plaque size reduction in ApoE–/–mice. Radiat Res. 2018;189(2):187–96.PubMedCrossRef Ebrahimian T, et al. Chronic exposure to external low-dose gamma radiation induces an increase in anti-inflammatory and anti-oxidative parameters resulting in atherosclerotic plaque size reduction in ApoE–/–mice. Radiat Res. 2018;189(2):187–96.PubMedCrossRef
154.
Zurück zum Zitat Shao T, et al. Physical activity and nutritional influence on immune function: an important strategy to improve immunity and health status. Front Physiol. 2021;12:751374.PubMedPubMedCentralCrossRef Shao T, et al. Physical activity and nutritional influence on immune function: an important strategy to improve immunity and health status. Front Physiol. 2021;12:751374.PubMedPubMedCentralCrossRef
155.
Zurück zum Zitat Myrehaug S, et al. Cardiac morbidity following modern treatment for Hodgkin lymphoma: supra-additive cardiotoxicity of doxorubicin and radiation therapy. Leuk Lymphoma. 2008;49(8):1486–93.PubMedCrossRef Myrehaug S, et al. Cardiac morbidity following modern treatment for Hodgkin lymphoma: supra-additive cardiotoxicity of doxorubicin and radiation therapy. Leuk Lymphoma. 2008;49(8):1486–93.PubMedCrossRef
156.
Zurück zum Zitat Veeragandham RS, Goldin MD. Surgical management of radiation-induced heart disease. Ann Thorac Surg. 1998;65(4):1014–9.PubMedCrossRef Veeragandham RS, Goldin MD. Surgical management of radiation-induced heart disease. Ann Thorac Surg. 1998;65(4):1014–9.PubMedCrossRef
157.
Zurück zum Zitat Heidenreich PA, et al. Asymptomatic cardiac disease following mediastinal irradiation. J Am Coll Cardiol. 2003;42(4):743–9.PubMedCrossRef Heidenreich PA, et al. Asymptomatic cardiac disease following mediastinal irradiation. J Am Coll Cardiol. 2003;42(4):743–9.PubMedCrossRef
158.
Zurück zum Zitat Adams MJ, et al. Cardiovascular status in long-term survivors of Hodgkin’s disease treated with chest radiotherapy. J Clin Oncol. 2004;22(15):3139–48.PubMedCrossRef Adams MJ, et al. Cardiovascular status in long-term survivors of Hodgkin’s disease treated with chest radiotherapy. J Clin Oncol. 2004;22(15):3139–48.PubMedCrossRef
159.
Zurück zum Zitat Larsen RL, et al. Electrocardiographic changes and arrhythmias after cancer therapy in children and young adults. Am J Cardiol. 1992;70(1):73–7.PubMedCrossRef Larsen RL, et al. Electrocardiographic changes and arrhythmias after cancer therapy in children and young adults. Am J Cardiol. 1992;70(1):73–7.PubMedCrossRef
160.
Zurück zum Zitat Lipshultz S, Sallan S. Cardiovascular abnormalities in long-term survivors of childhood malignancy. J Clin Oncol. 1993;11(7):1199–203.PubMedCrossRef Lipshultz S, Sallan S. Cardiovascular abnormalities in long-term survivors of childhood malignancy. J Clin Oncol. 1993;11(7):1199–203.PubMedCrossRef
161.
Zurück zum Zitat Abdullah CS, et al. Doxorubicin-induced cardiomyopathy associated with inhibition of autophagic degradation process and defects in mitochondrial respiration. Sci Rep. 2019;9(1):2002.PubMedPubMedCentralCrossRef Abdullah CS, et al. Doxorubicin-induced cardiomyopathy associated with inhibition of autophagic degradation process and defects in mitochondrial respiration. Sci Rep. 2019;9(1):2002.PubMedPubMedCentralCrossRef
162.
Zurück zum Zitat Karlstaedt A, et al. Glucose 6-phosphate accumulates via phosphoglucose isomerase inhibition in heart muscle. Circ Res. 2020;126(1):60–74.PubMedCrossRef Karlstaedt A, et al. Glucose 6-phosphate accumulates via phosphoglucose isomerase inhibition in heart muscle. Circ Res. 2020;126(1):60–74.PubMedCrossRef
163.
Zurück zum Zitat Ritterhoff J, et al. Metabolic remodeling promotes cardiac hypertrophy by directing glucose to aspartate biosynthesis. Circ Res. 2020;126(2):182–96.PubMedCrossRef Ritterhoff J, et al. Metabolic remodeling promotes cardiac hypertrophy by directing glucose to aspartate biosynthesis. Circ Res. 2020;126(2):182–96.PubMedCrossRef
164.
Zurück zum Zitat Agnetti G, et al. Modulation of mitochondrial proteome and improved mitochondrial function by biventricular pacing of dyssynchronous failing hearts. Circ Cardiovasc Genet. 2010;3(1):78–87.PubMedCrossRef Agnetti G, et al. Modulation of mitochondrial proteome and improved mitochondrial function by biventricular pacing of dyssynchronous failing hearts. Circ Cardiovasc Genet. 2010;3(1):78–87.PubMedCrossRef
165.
Zurück zum Zitat Young ME, et al. Proposed regulation of gene expression by glucose in rodent heart. Gene Regul Syst Bio. 2007;1:251–62.PubMedPubMedCentral Young ME, et al. Proposed regulation of gene expression by glucose in rodent heart. Gene Regul Syst Bio. 2007;1:251–62.PubMedPubMedCentral
166.
Zurück zum Zitat Stanley WC, Recchia FA, Lopaschuk GD. Myocardial substrate metabolism in the normal and failing heart. Physiol Rev. 2005;85(3):1093–129.PubMedCrossRef Stanley WC, Recchia FA, Lopaschuk GD. Myocardial substrate metabolism in the normal and failing heart. Physiol Rev. 2005;85(3):1093–129.PubMedCrossRef
167.
Zurück zum Zitat Lopaschuk GD, et al. Myocardial fatty acid metabolism in health and disease. Physiol Rev. 2010;90(1):207–58.PubMedCrossRef Lopaschuk GD, et al. Myocardial fatty acid metabolism in health and disease. Physiol Rev. 2010;90(1):207–58.PubMedCrossRef
168.
169.
Zurück zum Zitat Sutendra G, et al. A metabolic remodeling in right ventricular hypertrophy is associated with decreased angiogenesis and a transition from a compensated to a decompensated state in pulmonary hypertension. J Mol Med. 2013;91:1315–27.PubMedCrossRef Sutendra G, et al. A metabolic remodeling in right ventricular hypertrophy is associated with decreased angiogenesis and a transition from a compensated to a decompensated state in pulmonary hypertension. J Mol Med. 2013;91:1315–27.PubMedCrossRef
171.
Zurück zum Zitat Damiani RM, et al. Pathways of cardiac toxicity: comparison between chemotherapeutic drugs doxorubicin and mitoxantrone. Arch Toxicol. 2016;90:2063–76.PubMedCrossRef Damiani RM, et al. Pathways of cardiac toxicity: comparison between chemotherapeutic drugs doxorubicin and mitoxantrone. Arch Toxicol. 2016;90:2063–76.PubMedCrossRef
172.
Zurück zum Zitat Crouch M-L, et al. Cyclophosphamide leads to persistent deficits in physical performance and in vivo mitochondria function in a mouse model of chemotherapy late effects. PLoS ONE. 2017;12(7):e0181086.PubMedPubMedCentralCrossRef Crouch M-L, et al. Cyclophosphamide leads to persistent deficits in physical performance and in vivo mitochondria function in a mouse model of chemotherapy late effects. PLoS ONE. 2017;12(7):e0181086.PubMedPubMedCentralCrossRef
173.
Zurück zum Zitat Căinap SS, et al. The prognostic role of EBER in pediatric cancer. Rom J Morphol Embryol. 2015;56(4):1269–77.PubMed Căinap SS, et al. The prognostic role of EBER in pediatric cancer. Rom J Morphol Embryol. 2015;56(4):1269–77.PubMed
174.
Zurück zum Zitat Ewer MS, Ewer SM. Cardiotoxicity of anticancer treatments. Nat Rev Cardiol. 2015;12(9):547–58.PubMedCrossRef Ewer MS, Ewer SM. Cardiotoxicity of anticancer treatments. Nat Rev Cardiol. 2015;12(9):547–58.PubMedCrossRef
175.
Zurück zum Zitat Racil Z, et al. Mechanism of impaired glucose metabolism during nilotinib therapy in patients with chronic myelogenous leukemia. Haematologica. 2013;98(10): e124.PubMedPubMedCentralCrossRef Racil Z, et al. Mechanism of impaired glucose metabolism during nilotinib therapy in patients with chronic myelogenous leukemia. Haematologica. 2013;98(10): e124.PubMedPubMedCentralCrossRef
176.
Zurück zum Zitat Breccia M, et al. Impaired fasting glucose level as metabolic side effect of nilotinib in non-diabetic chronic myeloid leukemia patients resistant to imatinib. Leuk Res. 2007;31(12):1770–2.PubMedCrossRef Breccia M, et al. Impaired fasting glucose level as metabolic side effect of nilotinib in non-diabetic chronic myeloid leukemia patients resistant to imatinib. Leuk Res. 2007;31(12):1770–2.PubMedCrossRef
177.
Zurück zum Zitat Dreyling M, et al. Phosphatidylinositol 3-kinase inhibition by copanlisib in relapsed or refractory indolent lymphoma. J Clin Oncol. 2017;35(35):3898–905.PubMedCrossRef Dreyling M, et al. Phosphatidylinositol 3-kinase inhibition by copanlisib in relapsed or refractory indolent lymphoma. J Clin Oncol. 2017;35(35):3898–905.PubMedCrossRef
178.
Zurück zum Zitat Lipshultz SE, Alvarez JA, Scully RE. Anthracycline associated cardiotoxicity in survivors of childhood cancer. Heart. 2008;94(4):525–33.PubMedCrossRef Lipshultz SE, Alvarez JA, Scully RE. Anthracycline associated cardiotoxicity in survivors of childhood cancer. Heart. 2008;94(4):525–33.PubMedCrossRef
180.
Zurück zum Zitat Kerkelä R, et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med. 2006;12(8):908–16.PubMedCrossRef Kerkelä R, et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med. 2006;12(8):908–16.PubMedCrossRef
181.
182.
Zurück zum Zitat •• Russo M, et al. Metabolic aspects of anthracycline cardiotoxicity. Curr Treat Options Oncol. 2021;22:1–21. Article is highly recommended due to its importance in metabolic aspects of anthracycline-induced cardiotoxicity.CrossRef •• Russo M, et al. Metabolic aspects of anthracycline cardiotoxicity. Curr Treat Options Oncol. 2021;22:1–21. Article is highly recommended due to its importance in metabolic aspects of anthracycline-induced cardiotoxicity.CrossRef
184.
Zurück zum Zitat Pitt JM, et al. Resistance mechanisms to immune-checkpoint blockade in cancer: tumor-intrinsic and-extrinsic factors. Immunity. 2016;44(6):1255–69.PubMedCrossRef Pitt JM, et al. Resistance mechanisms to immune-checkpoint blockade in cancer: tumor-intrinsic and-extrinsic factors. Immunity. 2016;44(6):1255–69.PubMedCrossRef
186.
Zurück zum Zitat Khunger A, et al. New insights into mechanisms of immune checkpoint inhibitor-induced cardiovascular toxicity. Curr Oncol Rep. 2020;22:1–11.CrossRef Khunger A, et al. New insights into mechanisms of immune checkpoint inhibitor-induced cardiovascular toxicity. Curr Oncol Rep. 2020;22:1–11.CrossRef
188.
189.
Zurück zum Zitat Herbst RS, et al. Pembrolizumab versus docetaxel for previously treated, PD-L1-positive, advanced non-small-cell lung cancer (KEYNOTE-010): a randomised controlled trial. Lancet. 2016;387(10027):1540–50.PubMedCrossRef Herbst RS, et al. Pembrolizumab versus docetaxel for previously treated, PD-L1-positive, advanced non-small-cell lung cancer (KEYNOTE-010): a randomised controlled trial. Lancet. 2016;387(10027):1540–50.PubMedCrossRef
191.
Zurück zum Zitat Lesokhin AM, et al. Nivolumab in patients with relapsed or refractory hematologic malignancy: preliminary results of a phase Ib study. J Clin Oncol. 2016;34(23):2698.PubMedPubMedCentralCrossRef Lesokhin AM, et al. Nivolumab in patients with relapsed or refractory hematologic malignancy: preliminary results of a phase Ib study. J Clin Oncol. 2016;34(23):2698.PubMedPubMedCentralCrossRef
192.
Zurück zum Zitat Nayak L, et al. PD-1 blockade with nivolumab in relapsed/refractory primary central nervous system and testicular lymphoma. Blood. 2017;129(23):3071–3.PubMedPubMedCentralCrossRef Nayak L, et al. PD-1 blockade with nivolumab in relapsed/refractory primary central nervous system and testicular lymphoma. Blood. 2017;129(23):3071–3.PubMedPubMedCentralCrossRef
194.
Zurück zum Zitat Wang J, et al. PD-1 deficiency results in the development of fatal myocarditis in MRL mice. Int Immunol. 2010;22(6):443–52.PubMedCrossRef Wang J, et al. PD-1 deficiency results in the development of fatal myocarditis in MRL mice. Int Immunol. 2010;22(6):443–52.PubMedCrossRef
195.
Zurück zum Zitat Semper H, et al. Drug-induced myocarditis after nivolumab treatment in a patient with PDL1-negative squamous cell carcinoma of the lung. Lung Cancer. 2016;99:117–9.PubMedCrossRef Semper H, et al. Drug-induced myocarditis after nivolumab treatment in a patient with PDL1-negative squamous cell carcinoma of the lung. Lung Cancer. 2016;99:117–9.PubMedCrossRef
197.
Zurück zum Zitat Ji C, et al. Myocarditis in cynomolgus monkeys following treatment with immune checkpoint inhibitors immune checkpoint inhibitors induce myocarditis in monkeys. Clin Cancer Res. 2019;25(15):4735–48.PubMedCrossRef Ji C, et al. Myocarditis in cynomolgus monkeys following treatment with immune checkpoint inhibitors immune checkpoint inhibitors induce myocarditis in monkeys. Clin Cancer Res. 2019;25(15):4735–48.PubMedCrossRef
199.
Zurück zum Zitat Puzanov I, et al. Managing toxicities associated with immune checkpoint inhibitors: consensus recommendations from the Society for Immunotherapy of Cancer (SITC) Toxicity Management Working Group. J Immunother Cancer. 2017;5(1):1–28.PubMedPubMedCentralCrossRef Puzanov I, et al. Managing toxicities associated with immune checkpoint inhibitors: consensus recommendations from the Society for Immunotherapy of Cancer (SITC) Toxicity Management Working Group. J Immunother Cancer. 2017;5(1):1–28.PubMedPubMedCentralCrossRef
200.
Zurück zum Zitat Yeh ETH, Bickford CL. Cardiovascular complications of cancer therapy: incidence, pathogenesis, diagnosis, and management. J Am Coll Cardiol. 2009;53(24):2231–47.PubMedCrossRef Yeh ETH, Bickford CL. Cardiovascular complications of cancer therapy: incidence, pathogenesis, diagnosis, and management. J Am Coll Cardiol. 2009;53(24):2231–47.PubMedCrossRef
201.
Zurück zum Zitat Bloom MW, et al. Cancer therapy–related cardiac dysfunction and heart failure: part 1: definitions, pathophysiology, risk factors, and imaging. Circ Heart Fail. 2016;9(1):e002661.PubMedPubMedCentralCrossRef Bloom MW, et al. Cancer therapy–related cardiac dysfunction and heart failure: part 1: definitions, pathophysiology, risk factors, and imaging. Circ Heart Fail. 2016;9(1):e002661.PubMedPubMedCentralCrossRef
203.
Zurück zum Zitat Cardinale D, et al. Trastuzumab-induced cardiotoxicity: clinical and prognostic implications of troponin I evaluation. J Clin Oncol. 2010;28(25):3910–6.PubMedCrossRef Cardinale D, et al. Trastuzumab-induced cardiotoxicity: clinical and prognostic implications of troponin I evaluation. J Clin Oncol. 2010;28(25):3910–6.PubMedCrossRef
204.
Zurück zum Zitat Cardinale D, et al. Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation. 2004;109(22):2749–54.PubMedCrossRef Cardinale D, et al. Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation. 2004;109(22):2749–54.PubMedCrossRef
206.
Zurück zum Zitat Members ATF, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Euro Heart J. 2012;33(14):1787–847.CrossRef Members ATF, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Euro Heart J. 2012;33(14):1787–847.CrossRef
207.
Zurück zum Zitat De Iuliis F, et al. Serum biomarkers evaluation to predict chemotherapy-induced cardiotoxicity in breast cancer patients. Tumour Biol. 2016;37(3):3379–87.PubMedCrossRef De Iuliis F, et al. Serum biomarkers evaluation to predict chemotherapy-induced cardiotoxicity in breast cancer patients. Tumour Biol. 2016;37(3):3379–87.PubMedCrossRef
208.
Zurück zum Zitat Witteles R. Biomarkers as predictors of cardiac toxicity from targeted cancer therapies. J Card Fail. 2016;22(6):459–64.PubMedCrossRef Witteles R. Biomarkers as predictors of cardiac toxicity from targeted cancer therapies. J Card Fail. 2016;22(6):459–64.PubMedCrossRef
209.
Zurück zum Zitat Onitilo AA, et al. High-sensitivity C-reactive protein (hs-CRP) as a biomarker for trastuzumab-induced cardiotoxicity in HER2-positive early-stage breast cancer: a pilot study. Breast Cancer Res Treat. 2012;134(1):291–8.PubMedCrossRef Onitilo AA, et al. High-sensitivity C-reactive protein (hs-CRP) as a biomarker for trastuzumab-induced cardiotoxicity in HER2-positive early-stage breast cancer: a pilot study. Breast Cancer Res Treat. 2012;134(1):291–8.PubMedCrossRef
211.
Zurück zum Zitat Vejpongsa P, Yeh ETH. Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities. J Am Coll Cardiol. 2014;64(9):938–45.PubMedCrossRef Vejpongsa P, Yeh ETH. Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities. J Am Coll Cardiol. 2014;64(9):938–45.PubMedCrossRef
212.
Zurück zum Zitat Lyu YL, et al. Topoisomerase IIbeta mediated DNA double-strand breaks: implications in doxorubicin cardiotoxicity and prevention by dexrazoxane. Cancer Res. 2007;67(18):8839–46.PubMedCrossRef Lyu YL, et al. Topoisomerase IIbeta mediated DNA double-strand breaks: implications in doxorubicin cardiotoxicity and prevention by dexrazoxane. Cancer Res. 2007;67(18):8839–46.PubMedCrossRef
213.
Zurück zum Zitat Lipshultz SE, et al. Assessment of dexrazoxane as a cardioprotectant in doxorubicin-treated children with high-risk acute lymphoblastic leukaemia: long-term follow-up of a prospective, randomised, multicentre trial. Lancet Oncol. 2010;11(10):950–61.PubMedPubMedCentralCrossRef Lipshultz SE, et al. Assessment of dexrazoxane as a cardioprotectant in doxorubicin-treated children with high-risk acute lymphoblastic leukaemia: long-term follow-up of a prospective, randomised, multicentre trial. Lancet Oncol. 2010;11(10):950–61.PubMedPubMedCentralCrossRef
214.
Zurück zum Zitat Barbosa RR, et al. Anthracycline-associated cardiotoxicity in adults: systematic review on the cardioprotective role of beta-blockers. Rev Assoc Med Bras (1992). 2018;64:745–54.PubMedCrossRef Barbosa RR, et al. Anthracycline-associated cardiotoxicity in adults: systematic review on the cardioprotective role of beta-blockers. Rev Assoc Med Bras (1992). 2018;64:745–54.PubMedCrossRef
215.
Zurück zum Zitat Hutchins KK, et al. Prevention of cardiotoxicity among survivors of childhood cancer. Br J Clin Pharmacol. 2017;83(3):455–65.PubMedCrossRef Hutchins KK, et al. Prevention of cardiotoxicity among survivors of childhood cancer. Br J Clin Pharmacol. 2017;83(3):455–65.PubMedCrossRef
Metadaten
Titel
A Comprehensive Review of Cancer Drug–Induced Cardiotoxicity in Blood Cancer Patients: Current Perspectives and Therapeutic Strategies
verfasst von
Vincenzo Costanzo, PhD
Yashwant Kumar Ratre, PhD
Emanuela Andretta, PhD
Rakesh Acharya, M.sc Zoology
L. V. K. S. Bhaskar, PhD
Henu Kumar Verma, PhD
Publikationsdatum
19.02.2024
Verlag
Springer US
Erschienen in
Current Treatment Options in Oncology / Ausgabe 4/2024
Print ISSN: 1527-2729
Elektronische ISSN: 1534-6277
DOI
https://doi.org/10.1007/s11864-023-01175-z

Weitere Artikel der Ausgabe 4/2024

Current Treatment Options in Oncology 4/2024 Zur Ausgabe

Alphablocker schützt vor Miktionsproblemen nach der Biopsie

16.05.2024 alpha-1-Rezeptorantagonisten Nachrichten

Nach einer Prostatabiopsie treten häufig Probleme beim Wasserlassen auf. Ob sich das durch den periinterventionellen Einsatz von Alphablockern verhindern lässt, haben australische Mediziner im Zuge einer Metaanalyse untersucht.

Antikörper-Wirkstoff-Konjugat hält solide Tumoren in Schach

16.05.2024 Zielgerichtete Therapie Nachrichten

Trastuzumab deruxtecan scheint auch jenseits von Lungenkrebs gut gegen solide Tumoren mit HER2-Mutationen zu wirken. Dafür sprechen die Daten einer offenen Pan-Tumor-Studie.

Mammakarzinom: Senken Statine das krebsbedingte Sterberisiko?

15.05.2024 Mammakarzinom Nachrichten

Frauen mit lokalem oder metastasiertem Brustkrebs, die Statine einnehmen, haben eine niedrigere krebsspezifische Mortalität als Patientinnen, die dies nicht tun, legen neue Daten aus den USA nahe.

Labor, CT-Anthropometrie zeigen Risiko für Pankreaskrebs

13.05.2024 Pankreaskarzinom Nachrichten

Gerade bei aggressiven Malignomen wie dem duktalen Adenokarzinom des Pankreas könnte Früherkennung die Therapiechancen verbessern. Noch jedoch klafft hier eine Lücke. Ein Studienteam hat einen Weg gesucht, sie zu schließen.

Update Onkologie

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