Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia

To assess cardiac toxicity of anthracycline treatment with six biomarkers of cardiac injury: myoglobin, creatine kinase MB (CK-MB mass), cardiac troponin T (cTnT), cardiac troponin I (cTnI), heart-type fatty acid binding protein (H-FABP), glycogen phosphorylase BB (GPBB). Methods: We evaluated anthr...

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Дата:2008
Автори: Horacek, J.M., Tichy, M., Jebavy, L., Pudil, R., Ulrychova, M., Maly, J.
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Опубліковано: Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України 2008
Назва видання:Experimental Oncology
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Цитувати:Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia / J.M. Horacek, M. Tichy, L. Jebavy, R. Pudil, M. Ulrychova, J. Maly // Experimental Oncology. — 2008. — Т. 30, № 2. — С. 157–159. — Бібліогр.: 10 назв. — англ.

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spelling nasplib_isofts_kiev_ua-123456789-1391902025-02-09T14:53:56Z Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia Биомаркеры для оценки кардиотоксичности, вызванной антрациклином, у больных острой миелоидной лейкемией Horacek, J.M. Tichy, M. Jebavy, L. Pudil, R. Ulrychova, M. Maly, J. Uncategorized To assess cardiac toxicity of anthracycline treatment with six biomarkers of cardiac injury: myoglobin, creatine kinase MB (CK-MB mass), cardiac troponin T (cTnT), cardiac troponin I (cTnI), heart-type fatty acid binding protein (H-FABP), glycogen phosphorylase BB (GPBB). Methods: We evaluated anthracycline-induced cardiotoxicity in 12 acute myeloid leukemia patients (mean age 51.3 ± 10.7 years, 7 females). All biomarkers were measured at the baseline, after first chemotherapy (CT) with anthracyclines, after last CT with anthracyclines (total cumulative dose 479.8 ± 106.2 mg/m2) and 6 months thereafter. Values above the reference range were considered elevated. Results: GPBB increased above the cut-off (7.30 µg/L) in 2 (16.7%) patients after first CT, in 3 (25.0%) patients after last CT and remained elevated in 2 (16.7%) patients within 6 months after CT. CTnI became elevated (above 0.40 µg/L) in 1 (8.3%) patient after first and last CT and within 6 months after CT. CTnT remained negative (below 0.01 µg/L) during CT in all patients. Six months after CT, delayed cTnT positivity was found in 1 (8.3%) patient. All patients with cTnI or cTnT positivity had elevated GPBB. Other biomarkers (myoglobin, CK-MB mass, H-FABP) remained within the reference range in all patients. Conclusion: Our preliminary results suggest that GPBB could be a new promising marker for detection of anthracycline-related cardiotoxicity and probably superior to cardiac troponins. The predictive value for development of cardiomyopathy in the future is not clear and will be evaluated during a prospective follow-up. Цель: провести оценку кардиотоксичности, вызываемой антрациклином, с помощью ряда биомаркеров поражения сердца: миоглобина, креатин-киназы MB (CK-MB mass), кардиального тропонина T (cTnT), кардиального тропонина I (cTnI), белка, связывающего жирные кислоты (H-FABP), и гликогенфосфорилазы BB (GPBB). Методы: оценку кардиотоксичности проводили у 12 больных острой миелоидной лейкемией (средний возраст — 51,3 ± 10,7 года, 7 женщин). Измерены начальные показатели всех биомаркеров, а также таковые после проведения первой и последней химиотерапии (ХT) антрациклинами (общая накопленная доза — 479,8 ± 106,2 мг/м2 ) и через 6 мес после завершения терапии. Значения выше начальных рассматривали как повышенные. Результаты: уровень GPBB превысил норму (7,30 µg/L) у 2 больных (16,7%) после первой ХT, у 3 (25,0%) — после последней ХT и оставался повышенным у 2 больных (16,7%) и через 6 мес после ХT. Уровень CTnI повысился (более 0,40 µg/L) у 1 больного (8,3%) после первой и последней ХT, а также и через 6 мес после ХT. Значения CTnT оставались в пределах нормы (ниже 0,01 µg/L) во время проведения CT у всех пациентов. Через 6 мес после ХT отдаленная положительная реакция на cTnT выявлена у 1 больного (8,3%). У всех пациентов с положительными cTnI или cTnT установлен повышенный уровень GPBB. Другие биомаркеры (миоглобин, CK-MB, H-FABP) оставались в пределах нормы у всех больных. Выводы: предварительные результаты, полученные в данном исследовании, позволяют предположить, что GPBB можно рассматривать как новый перспективный маркер для выявления кардиотоксичности, вызванной антрациклинами, и, возможно, превосходит предложенные ранее тропонины. Возможная прогностическая ценность этого маркера при развитии кардиомиопатии пока не установлена. The study was supported by research projects MO 0FVZ 0000503 (Czech Ministry of Defence), MZO 00179906 (Czech Ministry of Health) and MSM 0021620817 (Czech Ministry of Education). 2008 Article Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia / J.M. Horacek, M. Tichy, L. Jebavy, R. Pudil, M. Ulrychova, J. Maly // Experimental Oncology. — 2008. — Т. 30, № 2. — С. 157–159. — Бібліогр.: 10 назв. — англ. 1812-9269 https://nasplib.isofts.kiev.ua/handle/123456789/139190 en Experimental Oncology application/pdf Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України
institution Digital Library of Periodicals of National Academy of Sciences of Ukraine
collection DSpace DC
language English
topic Uncategorized
Uncategorized
spellingShingle Uncategorized
Uncategorized
Horacek, J.M.
Tichy, M.
Jebavy, L.
Pudil, R.
Ulrychova, M.
Maly, J.
Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia
Experimental Oncology
description To assess cardiac toxicity of anthracycline treatment with six biomarkers of cardiac injury: myoglobin, creatine kinase MB (CK-MB mass), cardiac troponin T (cTnT), cardiac troponin I (cTnI), heart-type fatty acid binding protein (H-FABP), glycogen phosphorylase BB (GPBB). Methods: We evaluated anthracycline-induced cardiotoxicity in 12 acute myeloid leukemia patients (mean age 51.3 ± 10.7 years, 7 females). All biomarkers were measured at the baseline, after first chemotherapy (CT) with anthracyclines, after last CT with anthracyclines (total cumulative dose 479.8 ± 106.2 mg/m2) and 6 months thereafter. Values above the reference range were considered elevated. Results: GPBB increased above the cut-off (7.30 µg/L) in 2 (16.7%) patients after first CT, in 3 (25.0%) patients after last CT and remained elevated in 2 (16.7%) patients within 6 months after CT. CTnI became elevated (above 0.40 µg/L) in 1 (8.3%) patient after first and last CT and within 6 months after CT. CTnT remained negative (below 0.01 µg/L) during CT in all patients. Six months after CT, delayed cTnT positivity was found in 1 (8.3%) patient. All patients with cTnI or cTnT positivity had elevated GPBB. Other biomarkers (myoglobin, CK-MB mass, H-FABP) remained within the reference range in all patients. Conclusion: Our preliminary results suggest that GPBB could be a new promising marker for detection of anthracycline-related cardiotoxicity and probably superior to cardiac troponins. The predictive value for development of cardiomyopathy in the future is not clear and will be evaluated during a prospective follow-up.
format Article
author Horacek, J.M.
Tichy, M.
Jebavy, L.
Pudil, R.
Ulrychova, M.
Maly, J.
author_facet Horacek, J.M.
Tichy, M.
Jebavy, L.
Pudil, R.
Ulrychova, M.
Maly, J.
author_sort Horacek, J.M.
title Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia
title_short Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia
title_full Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia
title_fullStr Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia
title_full_unstemmed Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia
title_sort use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia
publisher Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України
publishDate 2008
topic_facet Uncategorized
url https://nasplib.isofts.kiev.ua/handle/123456789/139190
citation_txt Use of multiple biomarkers for evaluation of anthracycline-induced cardiotoxicity in patients with acute myeloid leukemia / J.M. Horacek, M. Tichy, L. Jebavy, R. Pudil, M. Ulrychova, J. Maly // Experimental Oncology. — 2008. — Т. 30, № 2. — С. 157–159. — Бібліогр.: 10 назв. — англ.
series Experimental Oncology
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fulltext Experimental Oncology ��� �������� ���� ���ne� ������ �������� ���� ���ne� �����ne� ���� ��� ��� Cardiotoxicity is a potentially serio�s complication of oncology treatment. Anthracyclines represent the greatest risk for development of cardiotoxicity [�]. Vario�s methods have been recommended for moni- toring of cardiotoxicity in oncology [�� �]. Recently� the applicability of cardiac troponins �cTnT� cTnI� and creatine kinase MB �CK-MB mass� has been investi- gated in this setting and the res�lts of clinical st�dies are inconsistent [4]. In several st�dies� no early ele- vations of cardiac troponins and CK-MB mass after administration of anthracyclines were fo�nd [���]. We therefore eval�ated the possible role of new perspec- tive biomarkers of myocardial ischemia and necro- sis — heart-type fatty acid binding protein �H-FABP� and glycogen phosphorylase BB �GPBB�� recently investigated in the diagnostics and risk stratification of ac�te coronary syndromes [����]. H-FABP is a rela- tively small cytoplasmic protein for oxidation of fatty acids that is q�ite specific for heart m�scle. Plasma H-FABP increases above the reference range within ��� h of the onset of myocardial inj�ry and ret�rns to normal within ����� h. GPBB is a glycogenolytic enzyme providing gl�cose for the myocardi�m. Af- ter glycogenolysis in the ischemic tiss�e� GPBB is released from the sarcoplasmic retic�l�m into the cytoplasm and then into the circ�lation thro�gh the damaged cell membrane. GPBB is released into the circ�lation ��4 h after myocardial inj�ry� ret�rning to normal within �4��6 h of damage occ�rring. In the ac�te coronary syndrome setting� both markers are regarded early markers of cardiac inj�ry d�e to ac�te myocardial ischemia. The main mechanism of cardiac inj�ry ca�sed by anticancer therapy is mainly non- ischemic and prior cyclic exposition to anthracycline agents may play a role �chronic and late cardiotoxicity�. Th�s� it is diffic�lt to estimate the kinetics of release of these biomarkers from cardiomyocytes in this set- ting. According to the available literat�re� there are no data on �sability of these biomarkers for detection of anthracycline-related cardiotoxicity. The aim of o�r pilot st�dy was to assess cardiac toxicity of anthracycline treatment with six biomar- kers of cardiac inj�ry: myoglobin� CK-MB mass� cTnT �Roche Diagnostics�� cTnI� H-FABP� GPBB �Randox Laboratories Ltd.�. Twelve patients �mean age ��.� ± ��.� years� � fe- males� with de novo ac�te myeloid le�kemia �� — AML M�� � — AML M4� � — AML M�� were st�died. The patients were treated with ��6 cycles of conventional use of MuLTIPLe BIoMARKeRs foR eVALuATIoN of ANTHRACYCLINe-INDuCeD CARDIoToXICITY IN PATIeNTs wITH ACuTe MYeLoID LeuKeMIA J.M. Horacek1, 4, M. Tichy2, 4, L. Jebavy1, 4, R. Pudil3, M. Ulrychova2, J. Maly1 12nd Department of Medicine — Clinical Hematology, University Hospital and Charles University, Faculty of Medicine in Hradec Kralove, Czech Republic 2 Institute of Clinical Biochemistry and Diagnostics, University Hospital and Charles University, Faculty of Medicine in Hradec Kralove, Czech Republic 3 1st Department of Medicine, University Hospital and Charles University, Faculty of Medicine in Hradec Kralove, Czech Republic 4 Department of Internal Medicine, University of Defence, Faculty of Military Health Sciences in Hradec Kralove, Czech Republic Aim: To assess cardiac toxicity of anthracycline treatment with six biomarkers of cardiac injury: myoglobin, creatine kinase MB (CK-MB mass), cardiac troponin T (cTnT), cardiac troponin I (cTnI), heart-type fatty acid binding protein (H-FABP), glycogen phosphorylase BB (GPBB). Methods: We evaluated anthracycline-induced cardiotoxicity in 12 acute myeloid leukemia patients (mean age 51.3 ± 10.7 years, 7 females). All biomarkers were measured at the baseline, after first chemotherapy (CT) with an- thracyclines, after last CT with anthracyclines (total cumulative dose 479.8 ± 106.2 mg/m2) and 6 months thereafter. Values above the reference range were considered elevated. Results: GPBB increased above the cut-off (7.30 µg/L) in 2 (16.7%) patients after first CT, in 3 (25.0%) patients after last CT and remained elevated in 2 (16.7%) patients within 6 months after CT. CTnI became elevated (above 0.40 µg/L) in 1 (8.3%) patient after first and last CT and within 6 months after CT. CTnT remained negative (below 0.01 µg/L) during CT in all patients. Six months after CT, delayed cTnT positivity was found in 1 (8.3%) patient. All pa- tients with cTnI or cTnT positivity had elevated GPBB. Other biomarkers (myoglobin, CK-MB mass, H-FABP) remained within the reference range in all patients. Conclusion: Our preliminary results suggest that GPBB could be a new promising marker for detection of anthracycline-related cardiotoxicity and probably superior to cardiac troponins. The predictive value for development of cardiomyopathy in the future is not clear and will be evaluated during a prospective follow-up. Key Words: cardiac biomarkers, glycogen phosphorylase BB, cardiotoxicity, anthracyclines, chemotherapy, acute myeloid leukemia. Received: March 16, 2008. *Correspondence: E-mail: jan.hor@post.cz Abbreviations used: CK-MB mass – creatine kinase MB; CT – chemotherapy; cTnI – cardiac troponin I; cTnT – cardiac troponin T; GPBB – glycogen phosphorylase BB; H-FABP – heart- type fatty acid binding protein. Exp Oncol ���� ��� �� ������� ��� Experimental Oncology ��� �������� ���� ���ne� chemotherapy �CT� containing anthracycline agent �idar�bicin� da�nor�bicin or mitoxantrone� in com- bination with cytarabine �so called “� + �” or “� + �” regimen� i. e. anthracycline agent for � or � days and cytarabine for � or � days per a cycle�. The stan- dard doses of anthracyclines for a cycle of CT were as follows: idar�bicin � x �� mg/m�� da�nor�bicin � x �� mg/m�� mitoxantrone ��� x �� mg/m�. To calc�- late the c�m�lative dose of anthracyclines� we applied conversion factors derived from the maxim�m recom- mended c�m�lative doses for individ�al agents �sed. The total c�m�lative dose of anthracyclines in o�r cohort reached 4��.� ± ��6.� mg/m�. Three patients were treated for arterial hypertension� other patients had no history of cardiovasc�lar disease. All patients had normal liver and renal f�nctions d�ring the st�dy. Biomarkers of cardiac inj�ry were meas�red on Elecsys Roche and Evidence Randox analyzers at the baseline �before CT�� the day after first CT with anthracyclines �after first CT� c�m�lative dose ��4.� ± ��.� mg/m��� the day after last CT with anthracyclines �after last CT� total c�m�lative dose 4��.� ± ��6.� mg/m�� and 6 months after completion of treatment �6 months after CT�. Concentrations of cardiac biomarkers di- agnostic for cardiotoxicity of anticancer therapy have not been established yet. In o�r st�dy� val�es above the reference range based on a n�mber of st�dies and recommended by the man�fact�rer were considered elevated. The c�t-off val�es for individ�al biomarkers were as follows: �6.� µg/L for myoglobin� 4.�� µg/L for CK-MB mass� �.�� µg/L for cTnT� �.4� µg/L for cTnI� 4.�� µg/L for H-FABP� �.�� µg/L for GPBB. The res�lts are shown in the Table. Before CT� all biomarkers of cardiac inj�ry were below the c�t-off val�es in all patients. GPBB concentrations increased above the c�t-off ��.�� µg/L� in � patients after first CT� in � patients after last CT and remained elevated in � patients within 6 months after CT. CTnI became elevated �above �.4� µg/L� in � patient after first CT and last CT and remained elevated within 6 months after CT. CTnT concentrations were negative �below �.�� µg/L� after first and last CT in all patients. Six months after completion of CT� we fo�nd delayed cTnT positivity in � patient. All patients with positivity of cTnI or cTnT had elevated GPBB as well. Other biomarkers �myoglobin� CK-MB mass� H-FABP� remained within the reference range in all patients. Table. Elevated biomarkers of cardiac injury in acute myeloid leukemia patients treated with anthracyclines (n = 12) Cardiac biomarkers Before CT After first CT After last CT 6 months after CT Myoglobin above 76.0 µg/L 0 0 0 0 CK-MB mass above 4.80 µg/L 0 0 0 0 cTnT above 0.01 µg/L 0 0 0 1 (8.3%) cTnI above 0.40 µg/L 0 1 (8.3%) 1 (8.3%) 1 (8.3%) H-FABP above 4.50 µg/L 0 0 0 0 GPBB above 7.30 µg/L 0 2 (16.7%) 3 (25.0%) 2 (16.7%) Notes: CT – chemotherapy; CK-MB mass – creatine kinase MB; cTnT – cardiac troponin T; cTnI – cardiac troponin I; H-FABP – heart-type fatty acid binding protein; GPBB – glycogen phosphorylase BB. O�r res�lts s�ggest that anthracycline treatment in ac�te myeloid le�kemia may be associated with myocardial inj�ry manifested by increased release of GPBB from cardiomyocytes� in o�r cohort in � ��6.�%� patients after first CT with anthracyclines and in � ���.�%� patients after last CT with anthracyclines� respectively. These findings co�ld be considered a sign of ac�te s�bclinical cardiotoxicity of anthracycline treatment. Persistent GPBB elevations in � ��6.�%� pa- tients within 6 months after completion of CT co�ld be a sign of chronic cardiac toxicity related to �ndergone oncology treatment. Whether these changes will have predictive val�e for treatment-related cardiomyopathy in the f�t�re is not clear and m�st be eval�ated d�r- ing a prospective follow-�p. According to o�r res�lts� GPBB seems to be a promising marker for eval�ation of anthracycline-ind�ced cardiotoxicity and probably s�perior to cardiac troponins �cTnI� cTnT� in this setting. Other biomarkers of cardiac inj�ry �H-FABP� CK-MB mass� myoglobin� do not seem to be of val�e in the detection of cardiotoxicity d�ring anthracycline treat- ment in ac�te myeloid le�kemia. F�rther st�dies in a larger n�mber of patients will be necessary to confirm o�r preliminary res�lts and define the potential role of new biomarkers in the eval�ation of treatment-related cardiotoxicity in oncology. ACKNowLeDGeMeNTs The st�dy was s�pported by research projects MO �FVZ ������� �Czech Ministry of Defence�� MZO �������6 �Czech Ministry of Health� and MSM ����6����� �Czech Ministry of Ed�cation�. RefeReNCes 1. Shan K, Lincoff AM, Young JB. Anthracycline-induced cardiotoxicity. Ann Intern Med 1996; 125: 47–58. 2. Meinardi MT, van der Graaf WT, van Veldhuisen DJ, et al. Detection of anthracycline-induced cardiotoxicity. Cancer Treat Rev 1999; 25: 237–47. 3. Ganz WI, Sridhar KS, Ganz SS, et al. Review of tests for monitoring doxorubicin-induced cardiomyopathy. Oncology 1996; 53: 461–70. 4. Sparano JA, Brown DL, Wolff AC. Predicting cancer therapy-induced cardiotoxicity. The role of troponins and other markers. Drug Saf 2002; 25: 301–11. 5. Fink FM, Genser N, Fink C, et al. Cardiac troponin T and creatine kinase MB mass concentrations in children receiving anthracycline chemotherapy. Med Pediatr Oncol 1995; 25: 185–9. 6. Clark SJ, Pippon M, Hemsworth S, et al. Cardiac tro- ponin T following anthracycline chemotherapy in children and adolescents. J Chemother 2007; 19: 332–4. 7. Horacek JM, Pudil R, Jebavy L, et al. Assessment of anthracycline-induced cardiotoxicity with biochemical mar- kers. Exp Oncol 2007; 29: 309–13. 8. Apple FS, Wu AH, Mair J, et al. Committee on Stan- dardization of Markers of Cardiac Damage of the IFCC. Fu- ture biomarkers for detection of ischemia and risk stratification in acute coronary syndrome. Clin Chem 2005; 51: 810–24. 9. Azzazy HM, Pelsers MM, Christenson RH. Unbound free fatty acids and heart-type fatty acid-binding protein: diagnostic assays and clinical applications. Clin Chem 2006; 52: 19–29. 10. Peetz D, Post F, Schinzel H, et al. Glycogen phospho- rylase BB in acute coronary syndromes. Clin Chem Lab Med 2005; 43: 1351–8. Experimental Oncology ��� �������� ���� ���ne� ������ �������� ���� ���ne� �����ne� ���� ��� ��� БИОМАРКЕРы ДЛЯ ОЦЕНКИ КАРДИОТОКСИЧНОСТИ, ВыЗВАННОЙ АНТРАЦИКЛИНОМ, у БОЛьНых ОСТРОЙ МИЕЛОИДНОЙ ЛЕЙКЕМИЕЙ Цель: провести оценку кардиотоксичности, вызываемой антрациклином, с помощью ряда биомаркеров поражения сердца: миоглобина, креатин-киназы MB (CK-MB mass), кардиального тропонина T (cTnT), кардиального тропонина I (cTnI), белка, связывающего жирные кислоты (H-FABP), и гликогенфосфорилазы BB (GPBB). Методы: оценку кардиотоксич- ности проводили у 12 больных острой миелоидной лейкемией (средний возраст — 51,3 ± 10,7 года, 7 женщин). Измерены начальные показатели всех биомаркеров, а также таковые после проведения первой и последней химиотерапии (ХT) ан-T) ан-) ан- трациклинами (общая накопленная доза — 479,8 ± 106,2 мг/м2) и через 6 мес после завершения терапии. Значения выше начальных рассматривали как повышенные. Результаты: уровень GPBB превысил норму (7,30 µg/L) у 2 больных (16,7%) после первой ХT, у 3 (25,0%) — после последней ХT и оставался повышенным у 2 больных (16,7%) и через 6 мес после ХT. Уровень CTnI повысился (более 0,40 µg/L) у 1 больного (8,3%) после первой и последней ХT, а также и через 6 мес после ХT. Значения CTnT оставались в пределах нормы (ниже 0,01 µg/L) во время проведения CT у всех пациентов. Через 6 мес после ХT отдаленная положительная реакция на cTnT выявлена у 1 больного (8,3%). У всех пациентов с положительными cTnI или cTnT установлен повышенный уровень GPBB. Другие биомаркеры (миоглобин, CK-MB, H-FABP) оставались в пределах нормы у всех больных. Выводы: предварительные результаты, полученные в данном исследовании, позволяют предположить, что GPBB можно рассматривать как новый перспективный маркер для выявления кардиотоксичности, вызванной антрациклинами, и, возможно, превосходит предложенные ранее тропонины. Возможная прогностическая ценность этого маркера при развитии кардиомиопатии пока не установлена. Ключевые слова: кардиальные биомаркеры, гликоген фосфорилаза BB, кардиотоксичность, антрациклины, химиотерапия, острая миелоидная лейкемия. Copyright © Experimental Oncology, 2008