Application of flow cytometry to molecular medicine: Detection of tumor necrosis factor-related apoptosis-inducing ligand receptors in acute myeloid leukaemia blasts

2005 ◽  
Author(s):  
Alessandra Cappellini ◽  
Irina Mantovani ◽  
Pier Tazzari ◽  
Tiziana Grafone ◽  
Giovanni Martinelli ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Tumor Necrosis Factor ◽  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Tumor Necrosis ◽  
Molecular Medicine ◽  
Ligand Receptors ◽  
Necrosis Factor ◽  
Acute Myeloid

Aberrant Expression of CD Markers in Acute Myeloid Leukaemia

2018 ◽  
Vol 2 (01) ◽  
pp. 14-16
Author(s):  
Abul Kalam Azad ◽  
Md. Rafiquzzaman Khan ◽  
ABM Hasan Habib ◽  
Md. Abdul Wadud Miah ◽  
Masuda Begum
Keyword(s):  
Flow Cytometry ◽  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Acute Leukaemia ◽  
Antigen Expression ◽  
Aberrant Expression ◽  
Female Ratio ◽  
Cd Antigen ◽  
Cd Markers ◽  
Acute Myeloid

Background: Aberrant expression of cluster differentiation (CD) antigen marker is associated with poor outcome of acute leukaemia. Objective: Aim of this study is to determine the frequency and pattern of aberrant expression of CD markers in acute myeloid leukaemia patients in Bangladesh. Methods: This retrospective data analysis was conducted in the Department of Haematology, Bangabandhu Sheikh Mujib Medical University (BSMMU) to assess the frequency of aberrant CD antigen expression in acute myeloid leukaemia from October 2016 to September 2017. During this period, we did one hundred flow cytometry of acute leukaemia patients and among them we found 48 acute myeloid Leukaemia (AML) who were included in this study. Result: Mean age of patients was 35 years (SD­ +14 years; Rang 3 to 50 years) with male: female ratio of 0.92. Four colour flow cytometry was done on fresh bone marrow aspirates and peripheral blood. Among 48 AML patients, aberrant CD expression was observed in 58% cases.  CD5 and cCD79a lymphoid markers were seen to be expressed in 32% cases of AML. Aberrant cCD3 and CD7 were expressed in 29% and 25% cases respectively and aberrant CD10, CD19, cCD22 were expressed in 11%, 3%, 3% cases acute myeloid leukaemia patients respectively. Conclusion: Aberrant CD antigen expression is not uncommon in AML patients of Bangladeshi population that may adversely affect the treatment outcome of the disease.

Involvement of tumor necrosis factor–related apoptosis-inducing ligand and tumor necrosis factor–related apoptosis-inducing ligand receptors in viral hepatic diseases

2005 ◽  
Vol 36 (10) ◽  
pp. 1066-1073 ◽  
Author(s):  
Yukiko Saitou ◽  
Katsuya Shiraki ◽  
Hiroyuki Fuke ◽  
Tomoko Inoue ◽  
Kazumi Miyashita ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Hepatic Diseases ◽  
Ligand Receptors ◽  
Necrosis Factor

Oroxylin a Heightens Tumor Necrosis Factor a-Induced Differentiation Effects on Acute Myeloid Leukemia Cells Via Modulation on AKT and NF-Kb Pathways Involving RXRa

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4840-4840
Author(s):  
Jingyan Xu ◽  
Jian Ouyang ◽  
Hui Hui
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tumor Necrosis Factor ◽  
Myeloid Leukemia ◽  
Tumor Necrosis ◽  
Conflicts Of Interest ◽  
Combination Group ◽  
Oroxylin A ◽  
Necrosis Factor ◽  
Acute Myeloid ◽  
Resistant Cells

Abstract Tumor necrosis factor alpha (TNFα) is a complicated cytokine which could induce differentiation of acute myeloid leukemia (AML) cells. We have found that Oroxylin A, a natural compound isolated from Scutellariae radix, markedly enhanced TNFα-induced NBT reduction and CD11b/CD14 expression of AML cells. Besides, Giemsa staining also displayed that the combination group induced U937-MDR cells to differentiate into monocyte-like cells yet NB4 and HL-60-resistant cells to granulocytic-like cells. Further study showed that TNFα induced PI3K subunit p85α binding to N-terminal truncated nuclear receptor RXRα (tRXRα) proteins and activating AKT. On the contrary, these could be inhibited by Oroxylin A through inhibiting interaction between tRXRα and p85α in NB4 and HL-60-resistant cells. Moreover, Oroxylin A inhibited the activation of NF-κB signaling and the DNA binding activity by TNFα proved by EMSA in these two AML cells. All these suggested that Oroxylin A was able to inhibit NF-κB signaling and RXRα-dependent AKT signaling, the negative effects of TNFα for AML therapy, suggesting that combination of Oroxylin A and TNFα might be a novel candidate for differentiation therapy for AML cells and required further investigation. Disclosures No relevant conflicts of interest to declare.

scholarly journals Comparison of flow cytometry and enzyme cytochemistry for the detection of myeloperoxydase in acute myeloid leukaemia: interests of a new positivity threshold

2003 ◽  
Vol 122 (2) ◽  
pp. 211-216 ◽  
Author(s):  
Régis Peffault de Latour ◽  
Ollivier Legrand ◽  
Delphine Moreau ◽  
Jean-Yves Perrot ◽  
Claude Marie Blanc ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Enzyme Cytochemistry ◽  
Acute Myeloid

scholarly journals Cytokines regulate HIV-1 replication and lymphocyte apoptosis in vitro

2013 ◽  
Vol 94 (6) ◽  
pp. 906-910 ◽  
Author(s):  
S V Boichuk ◽  
P D Dunaev ◽  
I G Mustafin
Keyword(s):  
Flow Cytometry ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Lymphocyte Apoptosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Hiv 1 ◽  
Necrosis Factor

Aim. To study the ability of cytokines - interleukin-2, interleukin-7 and tumor necrosis factor alpha to induce human immunodeficiency virus type 1 (HIV-1) replication and lymphocyte apoptosis in vitro. Methods. Peripheral blood mononuclears were separated by centrifugation on a ficoll paque solution specific density gradient. Lymphocytes were cultivated in RPMI 1640 medium with addition of L-glutamine, embryonal bovine serum, antibiotics and cytokines (interleukines-2, -4, -7, tumor necrosis factor alpha). To infect the lymphocytes, a laboratory strain of HIV-1 NL4-3 (NIH ResReag. Prog., USA) was used. HIV-1 replication was assessed by р24gag viral protein level in culture supernatants (ELISA) and its cytozolic level in lymphocytes (flow cytometry). Lymphocyte apoptosis was assessed by flow cytometry using the following parameters: (1) decrease of transmembrane mitochondrial potential; (2) increase in phosphatidyl serine molecules expression. Lymphocyte activation was assessed by CD25 and HLA-DR molecules expression (flow cytometry). Results. Cytokines induce the HIV-1 replication in lymphocytes in vitro. HIV-1 replication was noted only if inactivated lymphocytes were present in the culture. At the same time, lymphocytes not expressing the classical activation markers (CD25 and HLA-DR) were present among the lymphocytes producing HIV-1 indicating the possible alternative mechanism of HIV-1 replication, not dependent on cell activation. This fact might also be an evidence of viral replication processes in the pool of latently-infected lymphocytes, not expressing the classic activation markers. The abovementioned cytokines promote apoptotic death of uninfected lymphocytes in vitro, backing up the infected cells viability and thus promoting HIV-1 replication. Conclusion. Cytokines (interleukines-2, -4, -7, tumor necrosis factor alpha) which are known as factors supporting the immune system homeostasis and immune response formation, might also play a negative role in HIV-1 pathogenesis - induce HIV-1 replication in lymphocytes and, probably, lead to reactivation of the pool of latently-infected lymphocytes, deepening the lymphopenia and leading to disease progression.

scholarly journals Tumor necrosis factor alpha (TNF alpha) downregulates c-kit proto- oncogene product expression in normal and acute myeloid leukemia CD34+ cells via p55 TNF alpha receptors

Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2506-2514 ◽  
Author(s):  
E Khoury ◽  
C Andre ◽  
S Pontvert-Delucq ◽  
B Drenou ◽  
C Baillou ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Cd34 Cells ◽  
Alpha Receptors ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Acute Myeloid

Tumor necrosis factor alpha (TNF alpha), as a modulator of hematopoiesis, interacts with many growth factor receptors, such as interleukin-3, granulocyte-macrophage colony-stimulating factor (CSF), and granulocyte-CSF receptors. Here, we studied the interactions between TNF alpha and the stem cell factor (SCF) receptor, c-kit, in normal CD34+ hematopoietic progenitors and their leukemic counterpart, ie, acute myeloid leukemic (AML) CD34+ cells coexpressing c-kit antigen. The results showed that (1) incubation of normal bone marrow mononuclear cells with 200 U/mL rhTNF alpha for 20 hours induced a diminution of 31.2% +/- 5.2% of CD34+ cells coexpressing c-kit; (2) the same decrease was observed using purified CD34+ cells and, furthermore, their proliferative response to SCF was inhibited by 31.5% +/- 7.3% after exposure to TNF alpha; (3) similar experiments performed on CD34+ c-kit+ AML cells from 11 patients gave comparable results. Further analysis at the mRNA level indicated that TNF alpha decreased c-kit mRNA transcripts. Moreover, using monoclonal antibodies against the two types of TNF alpha receptors, p75 and p55, we showed that the downregulation of c-kit proto-oncogene product by TNF alpha, on normal and leukemic CD34+ cells, was exclusively mediated by the TNF alpha p55 receptor. Therefore, we conclude that TNF alpha acts as a downregulator of the SCF receptor expression.

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