Abstract
B cell-activating factor (BAFF), a proliferation-inducing ligand (APRIL) and apoptosis-inducing ligand (TRAIL) were demonstrated in several haematological diseases including acute myeloid leukemia (AML). Those cytokines are capable of activating a broad spectrum of intracellular signalling cascades that can either induce apoptosis or protect from programmed cell death. We have analysed BAFF, APRIL and TRAIL serum concentrations in 76 patients with newly diagnosed AML and 40 healthy volunteers. The values were significantly higher for APRIL and BAFF but lower for TRAIL compared to healthy volunteers. Induction therapy significantly reduced the values for BAFF and increased them for TRAIL. Moreover, the concentration of BAFF and APRIL was significantly lower and the concentration of TRAIL higher in a group of patients with complete remission compared to non-respondent AML patients. In addition, higher concentrations of BAFF and lower of TRAIL predicted a shorter overall survival, suggesting thereby an important prognostic marker and possible therapeutic target in AML.
Highlights
Acute myeloid leukaemia (AML) represents a group of clonal haematopoietic stem cell disorders in which both failure to differentiate and overproliferation in the stem cell compartment result in the accumulation of non-functional myeloid cells termed myeloblasts and loss of normal haematopoietic function
Pre-treatment AML patients had a significantly higher serum concentration compared to healthy volunteers for BAFF, 3,651.1 pg/ml (983.9–9151.4 pg/ml) versus 651.4 pg/ml (362.9– 1,122.3 pg/ml), p
Over the last few decades, countless attempts have been made at establishing prognostic markers capable of discriminating high-risk patients and at identifying a new complex network of cytokines that either promote or inhibit AML cell growth, progression and the development of drug resistance or sensitivity
Summary
Acute myeloid leukaemia (AML) represents a group of clonal haematopoietic stem cell disorders in which both failure to differentiate and overproliferation in the stem cell compartment result in the accumulation of non-functional myeloid cells termed myeloblasts and loss of normal haematopoietic function. The existence of receptors activated by the tumour necrosis factor alpha (TNF-α) was demonstrated for several haematological diseases, including AML cells [3, 4]. The cytokine TNF-α is capable of activating a broad spectrum of intracellular signalling cascades that can either induce apoptosis (e.g. activation of caspase-8) or protect various cell types from programmed cell death (e.g. nuclear factor-kappa B (NF-κB) pathway activation) [5]. NF-κB activation is predominantly responsible for the expression of anti-apoptotic genes. Some proapoptotic genes, including Fas ligand or TRAIL, TNF-κ and p53, are targeted by NF-κB too [6]
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