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Primary Effusion Lymphoma Cell Death Induced by Bortezomib and AG 490 Activates Dendritic Cells through CD91
by
Trivedi, Pankaj
, Di Renzo, Livia
, Santarelli, Roberta
, Frati, Luigi
, Conte, Valeria
, Cirone, Mara
, Lotti, Lavinia Vittoria
, Faggioni, Alberto
, Gonnella, Roberta
in
Antigens
/ Antineoplastic Agents
/ Antineoplastic Agents - pharmacology
/ Antitumor agents
/ Apoptosis
/ Biochemistry
/ Biology
/ Boronic Acids
/ Boronic Acids - pharmacology
/ Bortezomib
/ Calreticulin
/ Calreticulin - metabolism
/ Cancer
/ Cancer therapies
/ Cell activation
/ Cell death
/ Cell Line
/ Chemotherapy
/ Cytokines
/ Cytotoxicity
/ Dendritic Cells
/ Dendritic Cells - immunology
/ Drugs
/ Effusion
/ Endoplasmic reticulum
/ Health aspects
/ Heat shock proteins
/ HSP70 Heat-Shock Proteins
/ HSP70 Heat-Shock Proteins - metabolism
/ HSP90 Heat-Shock Proteins
/ HSP90 Heat-Shock Proteins - metabolism
/ Hsp90 protein
/ Humans
/ Immune response
/ Immune system
/ Immunogenicity
/ Immunology
/ Immunosuppressive agents
/ Immunotherapy
/ Inhibitor drugs
/ Janus kinase 2
/ Kinetics
/ Life Sciences
/ Ligands
/ Low Density Lipoprotein Receptor-Related Protein-1
/ Low Density Lipoprotein Receptor-Related Protein-1 - metabolism
/ Lymphoma
/ Lymphoma, Primary Effusion
/ Lymphoma, Primary Effusion - immunology
/ Medicine
/ Mortality
/ Non-Hodgkin's lymphomas
/ Pancreatic cancer
/ Peptides
/ Phagocytosis
/ Phagocytosis - immunology
/ Primary effusion lymphoma
/ Protein Transport
/ Protein Transport - drug effects
/ Proteins
/ Pyrazines
/ Pyrazines - pharmacology
/ Stat3 protein
/ Targeted cancer therapy
/ Transcription
/ Tyrphostins
/ Tyrphostins - pharmacology
2012
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Primary Effusion Lymphoma Cell Death Induced by Bortezomib and AG 490 Activates Dendritic Cells through CD91
by
Trivedi, Pankaj
, Di Renzo, Livia
, Santarelli, Roberta
, Frati, Luigi
, Conte, Valeria
, Cirone, Mara
, Lotti, Lavinia Vittoria
, Faggioni, Alberto
, Gonnella, Roberta
in
Antigens
/ Antineoplastic Agents
/ Antineoplastic Agents - pharmacology
/ Antitumor agents
/ Apoptosis
/ Biochemistry
/ Biology
/ Boronic Acids
/ Boronic Acids - pharmacology
/ Bortezomib
/ Calreticulin
/ Calreticulin - metabolism
/ Cancer
/ Cancer therapies
/ Cell activation
/ Cell death
/ Cell Line
/ Chemotherapy
/ Cytokines
/ Cytotoxicity
/ Dendritic Cells
/ Dendritic Cells - immunology
/ Drugs
/ Effusion
/ Endoplasmic reticulum
/ Health aspects
/ Heat shock proteins
/ HSP70 Heat-Shock Proteins
/ HSP70 Heat-Shock Proteins - metabolism
/ HSP90 Heat-Shock Proteins
/ HSP90 Heat-Shock Proteins - metabolism
/ Hsp90 protein
/ Humans
/ Immune response
/ Immune system
/ Immunogenicity
/ Immunology
/ Immunosuppressive agents
/ Immunotherapy
/ Inhibitor drugs
/ Janus kinase 2
/ Kinetics
/ Life Sciences
/ Ligands
/ Low Density Lipoprotein Receptor-Related Protein-1
/ Low Density Lipoprotein Receptor-Related Protein-1 - metabolism
/ Lymphoma
/ Lymphoma, Primary Effusion
/ Lymphoma, Primary Effusion - immunology
/ Medicine
/ Mortality
/ Non-Hodgkin's lymphomas
/ Pancreatic cancer
/ Peptides
/ Phagocytosis
/ Phagocytosis - immunology
/ Primary effusion lymphoma
/ Protein Transport
/ Protein Transport - drug effects
/ Proteins
/ Pyrazines
/ Pyrazines - pharmacology
/ Stat3 protein
/ Targeted cancer therapy
/ Transcription
/ Tyrphostins
/ Tyrphostins - pharmacology
2012
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Primary Effusion Lymphoma Cell Death Induced by Bortezomib and AG 490 Activates Dendritic Cells through CD91
by
Trivedi, Pankaj
, Di Renzo, Livia
, Santarelli, Roberta
, Frati, Luigi
, Conte, Valeria
, Cirone, Mara
, Lotti, Lavinia Vittoria
, Faggioni, Alberto
, Gonnella, Roberta
in
Antigens
/ Antineoplastic Agents
/ Antineoplastic Agents - pharmacology
/ Antitumor agents
/ Apoptosis
/ Biochemistry
/ Biology
/ Boronic Acids
/ Boronic Acids - pharmacology
/ Bortezomib
/ Calreticulin
/ Calreticulin - metabolism
/ Cancer
/ Cancer therapies
/ Cell activation
/ Cell death
/ Cell Line
/ Chemotherapy
/ Cytokines
/ Cytotoxicity
/ Dendritic Cells
/ Dendritic Cells - immunology
/ Drugs
/ Effusion
/ Endoplasmic reticulum
/ Health aspects
/ Heat shock proteins
/ HSP70 Heat-Shock Proteins
/ HSP70 Heat-Shock Proteins - metabolism
/ HSP90 Heat-Shock Proteins
/ HSP90 Heat-Shock Proteins - metabolism
/ Hsp90 protein
/ Humans
/ Immune response
/ Immune system
/ Immunogenicity
/ Immunology
/ Immunosuppressive agents
/ Immunotherapy
/ Inhibitor drugs
/ Janus kinase 2
/ Kinetics
/ Life Sciences
/ Ligands
/ Low Density Lipoprotein Receptor-Related Protein-1
/ Low Density Lipoprotein Receptor-Related Protein-1 - metabolism
/ Lymphoma
/ Lymphoma, Primary Effusion
/ Lymphoma, Primary Effusion - immunology
/ Medicine
/ Mortality
/ Non-Hodgkin's lymphomas
/ Pancreatic cancer
/ Peptides
/ Phagocytosis
/ Phagocytosis - immunology
/ Primary effusion lymphoma
/ Protein Transport
/ Protein Transport - drug effects
/ Proteins
/ Pyrazines
/ Pyrazines - pharmacology
/ Stat3 protein
/ Targeted cancer therapy
/ Transcription
/ Tyrphostins
/ Tyrphostins - pharmacology
2012
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Primary Effusion Lymphoma Cell Death Induced by Bortezomib and AG 490 Activates Dendritic Cells through CD91
Journal Article
Primary Effusion Lymphoma Cell Death Induced by Bortezomib and AG 490 Activates Dendritic Cells through CD91
2012
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Overview
To understand how cytotoxic agent-induced cancer cell death affects the immune system is of fundamental importance to stimulate immune response to counteract the high mortality due to cancer. Here we compared the immunogenicity of Primary Effusion Lymphoma (PEL) cell death induced by anticancer drug Bortezomib (Velcade) and Tyrphostin AG 490, a Janus Activated Kinase 2/signal trasducer and activator of transcription-3 (JAK2/STAT3) inhibitor. We show that both treatments were able to induce PEL apoptosis with similar kinetics and promote dendritic cells (DC) maturation. The surface expression of molecules involved in immune activation, namely calreticulin (CRT), heat shock proteins (HSP) 90 and 70 increased in dying cells. This was correlated with DC activation. We found that PEL cell death induced by Bortezomib was more effective in inducing uptake by DC compared to AG 490 or combination of both drugs. However the DC activation induced by all treatments was completely inhibited when these cells were pretreated with a neutralizing antiboby directed against the HSP90/70 and CRT common receptor, CD91. The activation of DC by Bortezomib and AG 490 treated PEL cells, as seen in the present study, might have important implications for a combined chemo and immunotherapy in such patients.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Antineoplastic Agents - pharmacology
/ Biology
/ Boronic Acids - pharmacology
/ Cancer
/ Dendritic Cells - immunology
/ Drugs
/ Effusion
/ HSP70 Heat-Shock Proteins - metabolism
/ HSP90 Heat-Shock Proteins - metabolism
/ Humans
/ Kinetics
/ Ligands
/ Low Density Lipoprotein Receptor-Related Protein-1
/ Low Density Lipoprotein Receptor-Related Protein-1 - metabolism
/ Lymphoma
/ Lymphoma, Primary Effusion - immunology
/ Medicine
/ Peptides
/ Protein Transport - drug effects
/ Proteins
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