Acute myeloid leukemia (AML) shows a high degree of heterogeneity owing to a variety of mutations and the mechanisms of leukemogenesis. This heterogeneity is often not reflected in standard treatment approaches which while providing predictable outcomes in the majority of patients fail in particular cases even with high-dose multiagent chemotherapy regimens. Further, the unselective effect of chemotherapy leads to high treatment-related toxicity and the enormous risk of infection during prolonged pancytopenia, preventing further dose escalation. Cytokines play a role in leukemogenesis, AML cell persistence and treatment outcome. In this review we highlight cytokine dependent mechanisms essential for AML cell survival and the role of single cytokines in leukemogenesis and allogeneic transplantation-related phenomena. Cytokine-related mechanisms of leukemogenesis, AML cell persistence and resistance to chemotherapy are complex. Modulation of the cytokine network can disrupt signalling pathway activation and overcome the high resistance to treatment. It may also increase the selectivity of AML treatment, reduce the overall treatment-related toxicity and improve outcomes of AML treatment in all age groups of patients. This review provides a deeper insight into these processes with focus on the most vulnerable step. Special attention is paid to the possibility of selective influence on defined cell populations for therapeutic target. We believe that modulating cytokine-dependent processes in AML is an approach that could be included in standard chemotherapeutic regimens for improving overall treatment outcome.

Chemotherapy (CT)-induced cardiotoxicity remains a topical problem in cancer survivors. Anthracyclines represent the greatest risk for development of cardiotoxicity [1]. Various methods including cardiac biomarkers have been recommended for monitoring of cardiotoxicity in oncology. The clinical studies using cardiac troponins for evaluation of anthracycline-induced cardiotoxicity brought inconsistent results [2–4]. In our previous study, we, as the first, applied new biomarkers of cardiac injury—glycogen phosphorylase BB (GPBB) and heart-type fatty acid-binding protein (H-FABP)—in the assessment of cardiac toxicity during high-dose CT followed by hematopoietic cell transplantation [5]. In our current study, we evaluated acute and chronic cardiotoxicity of anthracyclines with multiple biomarkers of cardiac injury: GPBB, H-FABP, cardiac troponin I (cTnI), cardiac troponin T (cTnT), creatine kinase MB (CK-MB mass) and myoglobin. GPBB and H-FABP have not been studied in this setting so far.

Cardiotoxicity is a well-known and potentially serious complication of anticancer therapy. Anthracycline-based chemotherapy represents the greatest risk. Early detection of cardiotoxicity is crucial for applying preventive and supportive therapeutic strategies. Various methods have been recommended for monitoring of cardiotoxicity. In our conditions, echocardiography and electrocardiography are routinely used. However, this approach shows low sensitivity for the early prediction of cardiomyopathy when the possibilities of appropriate management could still improve the patient's outcome. Recently, biomarkers of cardiac injury have been investigated in the assessment of chemotherapy-induced cardiotoxicity. Cardiospecific biomarkers, such as cardiac troponins, show high diagnostic efficacy in the early subclinical phase of the disease before the clinical onset of cardiomyopathy. Increase in their concentrations correlates with disease severity. As for natriuretic peptides, some studies, including ours, have shown promising results. Definitive evidence of their diagnostic and prognostic role in this context is still lacking and natriuretic peptides have not been routinely used for monitoring of cardiotoxicity in clinical practice. Other perspective biomarkers of cardiotoxicity in oncology are under study, especially heart-type fatty acid-binding protein (H-FABP) and glycogen phosphorylase BB (GPBB). Our studies using GPBB have provided encouraging results. However, the available data are limited and their practical use in this context cannot be recommended until their clinical efficacy is clearly defined. This review covers the current status of biomarkers for the early detection of anthracycline-induced cardiotoxicity. The authors present in brief, their own experience with multiple biomarkers in the detection of cardiotoxicity.

Background: The aim of our study was to monitor radiofrequency catheter ablation-induced myocardial damage by measuring high-sensitivity cardiac troponin T (hs-cTnT). Methods: Serum concentrations of hs-cTnT (Elecsys 2010 system, Roche) were measured in 73 healthy blood donors and serially in 27 patients who had samples taken both before and 24 h after radiofrequency ablation (RFA) for atrioventricular nodal re-entry tachycardia (AVNRT), atrial fibrillation (AF) or right atrial flutter (AFL). Results: Significant increases of hs-cTnT were seen in patients after RFA (AVNRT: P = 0.0115, AF: P = 0.0011, AFL: P = 0.0009). Postprocedural serum hs-cTnT correlated with the number of radiofrequency applications and with the duration of RFA procedure. Spearman's coefficient of rank correlation ( r) were as follows: hs-cTnT versus RFA duration: r = 0.771 ( P < 0.001); hs-cTnT versus number of pulses: r = 0.708 ( P < 0.001). Patients with the diagnosis of AVNRT had lower serum hs-cTnT concentration after RFA compared with AFL ( P < 0.0001) and AF ( P < 0.0001) patients. Conclusions: Our data indicate that RFA causes a significant increase of serum hs-cTnT concentration that could be used to monitor myocardial injury.