scholarly journals Interferon-β lipofection II. Mechanisms involved in cell death and bystander effect induced by cationic lipid-mediated interferon-β gene transfer to human tumor cells

2012 ◽  
Vol 19 (6) ◽  
pp. 420-430 ◽  
Author(s):  
M S Villaverde ◽  
M L Gil-Cardeza ◽  
G C Glikin ◽  
L M E Finocchiaro
Keyword(s):  
Cell Death ◽  
Gene Transfer ◽  
Tumor Cells ◽  
Bystander Effect ◽  
Human Tumor ◽  
Cationic Lipid ◽  
Interferon Β ◽  
Human Tumor Cells

Molecular characterization of immunogenic cell death triggered by the high hydrostatic pressure in human tumor cells.

2014 ◽  
Vol 32 (15_suppl) ◽  
pp. e14008-e14008
Author(s):  
Irena Moserova ◽  
Iva Truxova ◽  
Pierre-Francois Cartron ◽  
Jirina Bartunkova ◽  
Radek Spisek ◽  
...  
Keyword(s):  
Cell Death ◽  
Hydrostatic Pressure ◽  
Tumor Cells ◽  
Molecular Characterization ◽  
High Hydrostatic Pressure ◽  
Human Tumor ◽  
Immunogenic Cell Death ◽  
Human Tumor Cells

7, 8-diacetoxy-4-methylcoumarin induced cell death in human tumor cells is influenced by calreticulin

Biochimie ◽  
2011 ◽  
Vol 93 (3) ◽  
pp. 497-505 ◽  
Author(s):  
Amit Verma ◽  
Anant Narayan Bhatt ◽  
Abdullah Farooque ◽  
Suchit Khanna ◽  
Divya Khaitan ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Cells ◽  
Human Tumor ◽  
Human Tumor Cells

Interferon-β lipofection I. Increased efficacy of chemotherapeutic drugs on human tumor cells derived monolayers and spheroids

2012 ◽  
Vol 19 (7) ◽  
pp. 508-516 ◽  
Author(s):  
M S Villaverde ◽  
M L Gil-Cardeza ◽  
G C Glikin ◽  
L M E Finocchiaro
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Chemotherapeutic Drugs ◽  
Interferon Β ◽  
Human Tumor Cells

scholarly journals Retroviral vector-mediated transfer of the tumor necrosis factor alpha gene into human cancer cells restores an apoptotic cell death program and induces a bystander-killing effect

Blood ◽  
1996 ◽  
Vol 87 (6) ◽  
pp. 2486-2495 ◽  
Author(s):  
A Gillio Tos ◽  
A Cignetti ◽  
G Rovera ◽  
R Foa
Keyword(s):  
Cell Death ◽  
Tumor Cells ◽  
Tumor Necrosis ◽  
Human Tumor ◽  
Retroviral Vector ◽  
Human Tumor Cells ◽  
Necrosis Factor Alpha ◽  
Killing Effect ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNFalpha) may induce tumor cell death by apoptosis, the physiologic program of cell death usually lost during neoplastic progression. However, many tumor cells are resistant to its effect unless high doses are administered. By retroviral vector- mediated gene transfer, we have transduced the TNFalpha gene into the DNA of human tumor cells to investigate whether the indefinite neoplastic cell proliferation could be blocked and the lost physiologic program of cell death restored. Evidence is provided that high-TNFalpha- producing clones generated from a human lymphoma T-cell line (ST4) can undergo apoptosis following transduction of the TNFalpha gene. Internucleosomal DNA cleavage was documented by May-Grunwald-Giemsa and by propidium iodide staining, as well as by gel electrophoresis. The induced apoptotic phenomenon is TNFalpha-mediated, since it can be reverted following incubation with anti-TNFalpha monoclonal antibodies (MoAbs), and it occurs with cytokine levels released in the supernatant by the engineered cells much lower(>100 times) than those required to promote the same effect on parental ST4 cells following administration of exogenous recombinant TNFalpha. The process is associated with a downregulation of the apoptosis-preventing gene, bcl-2, while the expression of bax and p53, genes usually involved in promoting apoptosis, persists. Mixed-culture experiments performed coincubating TNFalpha-transduced and untransduced ST4 cells allowed documentation of a bystander-killing effect on the parental cells. This phenomenon still occurred at transduced to parental cell ratios as low as 1:20 and was blocked in the presence of an anti-TNFalpha MoAb. These findings indicated that TNFalpha may play a regulatory role in the proliferation of human tumor cells, and suggest potential new antitumor therapeutic strategies based on the direct delivery of the TNFalpha gene into cancer cells.

High hydrostatic pressure to induce immunogenic cell death in human tumor cells.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 3076-3076
Author(s):  
Iva Truxova ◽  
Jitka Fucikova ◽  
Irena Moserova ◽  
Simona Partlova ◽  
Jirina Bartunkova ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Hydrostatic Pressure ◽  
Tumor Cells ◽  
Cell Lines ◽  
Primary Tumor ◽  
High Hydrostatic Pressure ◽  
Human Tumor ◽  
Immunogenic Cell Death ◽  
Human Tumor Cells

3076 Background: Recent studies have identified molecular events characteristic of immunogenic cell death. These include surface exposure of calreticulin, HSP70 and HSP90, release of intranuclear HMGB1 and secretion of ATP from dying cells. Several chemotherapeutic agents, including anthracyclins, oxaliplatin and bortezomib, and hypericin-based photodynamic therapy have been described to induce the immunogenic cell death in human tumor cells. We investigated the potential of high hydrostatic pressure (HHP) to induce immunogenic cell death in human tumor cells. Methods: Prostate and ovarian cancer cell lines and primary tumor cells were treated by HHP and we analyzed the kinetics of the expression of immunogenic cell death markers. HHP killed tumor cells expressing immunogenic cell death markers were tested for their ability to activate dendritic cells (DCs), to induce tumor specific T cells and regulatory T cells. Results: HHP induced rapid expression of HSP70, HSP90 and calreticulin on the cell surface of all tested cell lines and primary tumor cells. HHP also induced release of HMGB1 and ATP from treated cells. The kinetics of expression was similar to doxorubicin, HHP, however, induced 1.5-2 fold higher expression of HSP70, HSP90 and calreticulin. The interaction of DCs with HHP-treated tumor cells led to the faster rate of phagocytosis, significant upregulation of CD83, CD86 and HLA-DR and release of IL-6, IL-12p70 and TNFα. The ability of HHP-killed tumor cells to promote DCs maturation was cell contact dependent. DCs pulsed with tumor cells killed by HHP induced high numbers of tumor-specific CD4+ and CD8+IFN-g-producing T cells even in the absence of additional maturation stimulus. DCs pulsed with HHP treated tumor cells also induced the lowest number of regulatory T cells among the tested conditions. Cells treated by HHP can by cryopreserved in liquid nitrogen and retain their immunogenic properties upon thawing thus allowing for their convenient use in the manufacturing of cancer immunotherapy products. Conclusions: High hydrostatic pressure is a reliable and very potent inducer of immunogenic cell death in the wide range of human tumor cell lines and primary tumor cells.

In vivo validation of the bystander effect

2004 ◽  
Vol 23 (2) ◽  
pp. 71-73 ◽  
Author(s):  
Amin I Kassis
Keyword(s):  
Tumor Cells ◽  
Bystander Effect ◽  
Therapeutic Potential ◽  
Human Tumor ◽  
Alpha Particles ◽  
Medical Procedures ◽  
Human Tumor Cells ◽  
Biologic Response ◽  
In Vivo Validation

The bystander effect post radionuclide decay describes the biologic response(s) of cells not directly targeted by the radiation insult. Recently, we demonstrated that the specific irradiation of human tumor cells in vivo leads to a bystander effect in subcutaneously growing tumors. These in vivo findings 1) call for the re-evaluation of approaches currently used for estimating the risks to individuals/populations inadvertently exposed internally to radioactivity (e.g., alpha particles) as well as to patients undergoing routine diagnostic nuclear medical procedures, and 2) impact significantly the current dogma for assessing the therapeutic potential of internally administered radionuclides.

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