Cytokine profiles in acute myeloid leukemia patients at diagnosis: Survival is inversely correlated with IL-6 and directly correlated with IL-10 levels

Sánchez-Correa, Beatriz; Bergua, Juan; Campos, Carmen; Gayoso, Inmaculada; Arcos, María José; Bañas, Helena; Morgado, Sara; Casado, Javier G.; Solana, Rafael; Tarazona, Raquel

doi:10.1016/j.cyto.2012.12.023

Cited by 164 publications

(145 citation statements)

References 49 publications

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“…The knowledge gained from multi-analytical determination of cytokines and adhesion molecules could allow better diagnosis and management of hematological malignancies, since cytokines or their receptors may also represent a target for specific anticancer therapy at the molecular level. Recently, some studies reported the possible diagnostic and prognostic use of cytokine levels in newly diagnosed acute leukemias and myelodysplastic syndromes [10][11][12][13][14] . The aim of our pilot study was to evaluate serum profile of multiple cytokines and adhesion molecules in patients with newly diagnosed AML and ALL using the innovative biochip array technology.…”

Section: Introductionmentioning

confidence: 99%

Serum cytokine and adhesion molecule profile differs in newly diagnosed acute myeloid and lymphoblastic leukemia

Horáček¹,

Kupsa²,

Vašatová³

et al. 2015

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Aims.To compare serum levels of 17 cytokines and 5 adhesion molecules in patients with newly diagnosed acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) using biochip array technology. Methods. A total of 15 AML and 15 ALL patients were studied. Serum samples were taken prior to anticancer therapy and were analyzed by biochip based immunoassays on the Evidence Investigator analyzer. This approach allows simultaneous detection of multiple analytes from a single sample. T-tests were used for statistical analysis. Results. Comparing cytokine and adhesion molecules levels in newly diagnosed AML and ALL patients, we found significant increase in AML in serum IL-4 (P < 0.0001), IL-2 (P < 0.01), IL-3 (P < 0.05), and significant decrease (P < 0.05) in serum VEGF and VCAM-1. Discussion. Our results indicate that serum profile of cytokines and adhesion molecules differs in newly diagnosed AML and ALL patients. Further studies are needed to establish if these alterations could be used as a clinically relevant biomarker for acute leukemias.

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Section: Introductionmentioning

confidence: 99%

Serum cytokine and adhesion molecule profile differs in newly diagnosed acute myeloid and lymphoblastic leukemia

Horáček¹,

Kupsa²,

Vašatová³

et al. 2015

BIOMED PAP

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“…Hodgkin´s lymphoma, testicular, early breast and prostate cancer) and curative treatment, younger patients also suffer from secondary AML. In a recently published study on adult AML patients, the IL-6 levels inversely and IL-10 levels directly correlated with survival 25 . CRP levels were not evaluated in that study.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of cytokines and soluble adhesion molecules in patients with newly diagnosed acute myeloid leukemia: the role of TNF-alpha and FLT3-ITD

Kupsa¹,

Vaněk²,

Vašatová³

et al. 2016

BIOMED PAP

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Objectives. Acute myeloid leukemia (AML) cells are highly resistant to therapy. The presumed molecular basis of this resistance is the effect of tumor necrosis factor alpha (TNF-α) and other cytokines on endothelial adhesion molecule expression. The aim of this study was to test the hypothesis that cytokines and soluble adhesion molecules correlate in AML. Methods. Baseline serum levels of 17 cytokines and 5 soluble adhesion molecules were measured in 53 AML patients using biochip array technology. Age, leukocyte count, secondary AML, CRP, FLT3-ITD and remission were variables. Statistical analysis was performed in R version 3.1.2. Results. VCAM-1 correlated with ICAM-1 (P < 0.0001), E-selectin (P < 0.0001), leukocyte count (P = 0.0005) and TNF-α (P = 0.0035). E-selectin correlated with leukocyte count (P < 0.0001), P-selectin (P = 0.0032) and MCP-1 (P = 0.0119). CRP correlated with IL-6 (P < 0.0001), leukocyte count negatively correlated with IL-7 (P = 0.0318). FLT3-ITD was associated with higher E-selectin (P = 0.0010) and lower IL-7 (P = 0.0252). Secondary AML patients were older. Failure of induction therapy was associated with significantly higher CRP and lower P-selectin. Leukocyte count (P < 0.0001), FLT3-ITD (P = 0.0017) and secondary AML (P = 0.0439) influenced the principal component. Conclusions. Leukemic cells can modulate the microenvironment. Cytokine, adhesion molecule levels and leukocyte count correlate in AML. Understanding these mechanisms may form the basis of novel therapeutic approaches.

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“…An exciting possibility might be to target Tgfb since in an animal model it was demonstrated that a Tgfb monoclonal antibody prevented AML cell accumulation, worked in combination with cytarabine, and inhibited AML cell migration due to the prevention of Tgfb-induced CXCR4/CXCL12 activation [88]. IL6, too, might be a suitable and up to date target since high IL-6 levels have been associated with a poor clinical outcome and refractory disease [66] and humanized monoclonal antibodies against the IL-6 receptor are nowadays available. Recently, it has been observed that TNF-a released from stromal cells might be minimal, but this cytokine along with a high proteasome activity is critical for maintaining the constitutive activation of nuclear factor Kb (NFkB) in LICs but not in HSCs and non-LIC fractions of AML cells [67].…”

Section: Potential Targetsmentioning

confidence: 99%

“…It is well-known that MSCs actively participate in the "angiogenic switch" not only by releasing various angiogenic factors [62], but also by recruiting circulating vascular progenitor cells [63]. MSCs may inhibit adaptive and innate immunity by releasing immunosuppressive cytokines and effectors including tumor necrosis a (TNF-a) and interferon-g (IFN-g) either directly or under the influence of leukemic cells [64][65][66][67]. In addition, under the influence of Axl-expressing leukemic cells, BM derived MSCs are induced to express and produce the Axl ligand, i.e.…”

Section: Aml Cells Remodel the Nichementioning

confidence: 99%

Therapeutically targeting SELF‐reinforcing leukemic niches in acute myeloid leukemia: A worthy endeavor?

et al. 2016

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A tight relationship between the acute myeloid leukemia (AML) population and the bone marrow (BM) microenvironment has been convincingly established. The AML clone contains leukemic stem cells (LSCs) that compete with normal hematopoietic stem cells (HSCs) for niche occupancy and remodel the niche; whereas, the BM microenvironment might promote AML development and progression not only through hypoxia and homing/adhesion molecules, but also through genetic defects. Although it is still unknown whether the niche influences treatment results or contains any potential target for treatment, this dynamic AML-niche interaction might be a promising therapeutic objective to significantly improve the AML cure rate.

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Cytokine profiles in acute myeloid leukemia patients at diagnosis: Survival is inversely correlated with IL-6 and directly correlated with IL-10 levels

Cited by 164 publications

References 49 publications

Serum cytokine and adhesion molecule profile differs in newly diagnosed acute myeloid and lymphoblastic leukemia

Serum cytokine and adhesion molecule profile differs in newly diagnosed acute myeloid and lymphoblastic leukemia

Evaluation of cytokines and soluble adhesion molecules in patients with newly diagnosed acute myeloid leukemia: the role of TNF-alpha and FLT3-ITD

Therapeutically targeting SELF‐reinforcing leukemic niches in acute myeloid leukemia: A worthy endeavor?

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