Nonleukemic myeloid dendritic cells obtained from autologous stem cell products elicit antileukemia responses in patients with acute myeloid leukemia

Serrano‐López, Juana; Sánchez‐García, Joaquín; Serrano, Josefina; Alvarez‐Rivas, Miguel A.; García-Castellano, José Manuel; Román‐Gómez, José; Rosa, Olga de la; C, Herrera-Arroyo; Torres-Gomez, A

doi:10.1111/j.1537-2995.2010.03042.x

Cited by 9 publications

(3 citation statements)

References 35 publications

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“…The inhibitory effects of CCL3 on proliferation of AML cells were also reported by Owen-Lynch et al, [17]. Compelling evidences have also emphasized that, the expression of CCR5 is disrupted in leucocytes obtained from AML patients leukocytes [14,18,19], hence, it seems that CCR5/ligands interaction could be considered as a predominant mechanism which is disrupted in AML and probably is involved in the disease pathogenesis. Again, based on our results, it is likely that CCR5-D32 mutation probably dose not affect the CCR5 expression in our study AML patients and other genetical and epigenetical factors such as polymorphisms, methylation and acetylation of CCR5 gene as well as inhibitory effects of micro-RNA can be considered for future investigation.…”

Section: Discussionmentioning

confidence: 61%

Lack of Correlation Between the CCR5-Δ32 Mutation and Acute Myeloid Leukemia in Iranian Patients

Khorramdelazad

Mortazavi

Momeni

et al. 2014

Indian J Hematol Blood Transfus

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Chemokines and their receptors are crucially important in the pathogenesis of acute myeloblastic leukemia (AML). The CC chemokine receptor 5 (CCR5) is a specific chemokine receptor for CC chemokine ligand 3 (CCL3), CCL4 and CCL5 which all play key roles in identifying cancer properties and localization of leukemia cells. It has been demonstrated that the known mutation in CCR5 gene (CCR5-Δ32) leads to mal-expression of the receptor and affect its function. The aim of this study was to determine the rate of CCR5-Δ32 mutation within Iranian AML patients. In this study, blood samples were obtained from 60 AML patients and 300 healthy controls. The CCR5-Δ32 mutation was evaluated using Gap-PCR technique. Our results showed that CCR5-Δ32 mutation was not found in the patients, while three out of the controls had hetrozygotic form of this mutation. The rest of studied samples had the wild form of the gene. According to these findings, it can probably be concluded that the CCR5-Δ32 is not associated with susceptibility to AML in Iranian patients.

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Section: Discussionmentioning

confidence: 61%

Lack of Correlation Between the CCR5-Δ32 Mutation and Acute Myeloid Leukemia in Iranian Patients

Khorramdelazad

Mortazavi

Momeni

et al. 2014

Indian J Hematol Blood Transfus

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“…Conventional cytogenetic investigations, fluorescence in situ hybridization and molecular studies for NPM1 mutations and FLT3-ITD were performed as previously described. 19 Seventy-five patients suitable for intensive treatment received chemotherapy induction regimens based on PETHEMA Spanish Cooperative group protocols. Samples had been acquired during routine diagnostic assessments and were analyzed in accordance with the regulations and protocols approved by the "Reina Sofia" University Hospital.…”

Section: Methodsmentioning

confidence: 99%

Cytoplasmic localization of wild-type survivin is associated with constitutive activation of the PI3K/Akt signaling pathway and represents a favorable prognostic factor in patients with acute myeloid leukemia

et al. 2013

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© F e r r a t a S t o r t i F o u n d a t i o n 2 0 1 3and proliferative effects partially by increasing survivin levels through PI3K activation in AML. 15 Additionally, it has been shown in a mouse model that internal tandem duplication of Flt-3 regulates survivin expression via PI3K/Akt leading to aberrant progenitor cell proliferation. 16 Although the importance of the PI3K/Akt/survivin pathway has been reported in lung and colon cancer, 17,18 its incidence and prognostic impact in AML have not been described.In this study we analyzed the subcellular compartment distribution of WT survivin and the splicing variants survivin-2B and survivin-Delta-Ex3 in AML patients, the correlation with PI3K/Akt pathway activation, and the possible impact on outcome. MethodsWe included 105 consecutive patients diagnosed with AML between February 2006 and October 2010 in our institution. These patients' clinical features, biological characteristics and outcomes are listed in Table 1. Conventional cytogenetic investigations, fluorescence in situ hybridization and molecular studies for NPM1 mutations and FLT3-ITD were performed as previously described.19 Seventy-five patients suitable for intensive treatment received chemotherapy induction regimens based on PETHEMA Spanish Cooperative group protocols. Samples had been acquired during routine diagnostic assessments and were analyzed in accordance with the regulations and protocols approved by the "Reina Sofia" University Hospital. Informed consent had been obtained in accordance with the Declaration of Helsinki. For in vitro experiments, K562, HL-60 and MV4-11 leukemia cell lines were used (purchased from American Tissue Cell Culture, ATCC). Preparation of cytosolic and nuclear protein extractsCytosolic, membrane and nuclear proteins were sequentially isolated from mononuclear cells from bone marrow aspirates obtained at diagnosis, using a Q-proteome Cell Compartment kit (Qiagen Iberia SL, Madrid, Spain) according to the manufacture's instructions. Western blottingWT survivin and splicing variants were clearly distinguished by their different molecular weights: 16.5 KDa for the WT protein, 18 KDa for the 2B variant and 14 KDa for the Delta-Ex3 variant. The specificity of each isoform was further confirmed by blocking peptide experiments (Online Supplementary Figure S1). Cytosolic and nuclear specific fractions were tested for purity using anti-β actin (1:1000, Cell Signaling) and lamin-A (H-102, 1:500; Santa Cruz Biotechnology, Santa Cruz, CA, USA) (Online Supplementary Figure S2). Proteins were detected by chemiluminescence using a Chemigenius-2 device and quantified using Gene-Tools 5 analysis software (both from Syngene, Cambridge, UK) using β-actin or laminin as the loading control for cytoplasmic and nuclear extracts, respectively. Analysis of G0 quiescent and cell cycleFresh leukemic cells were first stained with fluorescein isothio-J. Serrano-López et al. 1878 haematologica | 2013; 98(12) Statistical analysisNormalized values of WT survivin and isoforms were...

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“…Our data are in accordance with observations from other groups. PBSCs obtained for autologous stem cell transplantation can constitute a novel source of MDCs to design feasible vaccination trials [ 59 ], [ 60 ]. DC-based vaccines against AML could be improved by CD25 T cell depletion allowing the induction of a long-lasting T cell response [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

Pulsing with blast cell lysate or blast-derived total RNA reverses the dendritic cell-mediated cytotoxic activity of cytokine-induced killer cells against allogeneic acute myelogenous leukemia cells

Schöttker¹,

Schmidt‐Wolf²

2011

GMS German Medical Science; 9:Doc18; ISSN 1612-3174

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Nonleukemic myeloid dendritic cells obtained from autologous stem cell products elicit antileukemia responses in patients with acute myeloid leukemia

Abstract: We conclude that PBSCs obtained for autologous stem cell transplantation can constitute a novel source of MDCs to design feasible vaccination trials.

Cited by 9 publications

References 35 publications

Lack of Correlation Between the CCR5-Δ32 Mutation and Acute Myeloid Leukemia in Iranian Patients

Lack of Correlation Between the CCR5-Δ32 Mutation and Acute Myeloid Leukemia in Iranian Patients

Cytoplasmic localization of wild-type survivin is associated with constitutive activation of the PI3K/Akt signaling pathway and represents a favorable prognostic factor in patients with acute myeloid leukemia

Pulsing with blast cell lysate or blast-derived total RNA reverses the dendritic cell-mediated cytotoxic activity of cytokine-induced killer cells against allogeneic acute myelogenous leukemia cells

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