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  1. Article ; Online: Corrigendum to "Silencing adenosine A2a receptor enhances dendritic cell-based cancer immunotherapy" [Nanomedicine Nanotechnol Biol Med 29 (2020) 102240].

    Masjedi, Ali / Ahmadi, Armin / Ghanee, Sepideh / Malakotikhah, Farinaz / Afjadi, Mohsen Nabi / Irandoust, Mahzad / Kiani, Fariba Karoon / Asl, Sima Heydarzadeh / Atyabi, Fatemeh / Hassannia, Hadi / Hojjat-Farsangi, Mohammad / Namdar, Afshin / Ghalamfarsa, Ghasem / Jadidi-Niaragh, Farhad

    Nanomedicine : nanotechnology, biology, and medicine

    2023  Volume 51, Page(s) 102690

    Language English
    Publishing date 2023-05-09
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 2183417-9
    ISSN 1549-9642 ; 1549-9634
    ISSN (online) 1549-9642
    ISSN 1549-9634
    DOI 10.1016/j.nano.2023.102690
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  2. Article: Silencing of p68 and STAT3 synergistically diminishes cancer progression

    Hashemi, Vida / Ahmadi, Armin / Malakotikhah, Farinaz / Chaleshtari, Mitra Ghasemi / Baghi Moornani, Mahdi / Masjedi, Ali / Sojoodi, Mozhdeh / Atyabi, Fatemeh / Nikkhoo, Afshin / Rostami, Narges / Baradaran, Behzad / Azizi, Gholamreza / Yousefi, Bahman / Ghalamfarsa, Ghasem / Jadidi-Niaragh, Farhad

    Life sciences. 2020 May 15, v. 249

    2020  

    Abstract: Since several factors are involved in the tumorigenesis process, targeting only one factor most probably cannot overwhelm cancer progression. Therefore, it seems that combination therapy through targeting more than one cancer-related factor may lead to ... ...

    Abstract Since several factors are involved in the tumorigenesis process, targeting only one factor most probably cannot overwhelm cancer progression. Therefore, it seems that combination therapy through targeting more than one cancer-related factor may lead to cancer control. The expression and function of p68 (DDX5; DEAD-Box Helicase 5) are dysregulated in various cancers. P68 is also a co-activator of many oncogenic transcription factors such as the signal transducer and activator of transcription-3 (STAT3), which contributes to cancer progression. This close connection between p68 and STAT3 plays an important role in the growth and development of cancer.We decided to suppress the p68/STAT3 axis in various cancer cells by using Polyethylene glycol-trimethyl Chitosan-Hyaluronic acid (PEG-TMC-HA) nanoparticles (NPs) loaded with siRNA molecules. We assessed the impact of this combination therapy on apoptosis, proliferation, angiogenesis, and tumor growth, both in vitro and in vivo.The results showed that siRNA-loaded NPs notably suppressed the expression of p68/STAT3 axis in cancer cells, which was associated with blockade of tumor growth, colony formation, angiogenesis, and cancer cell migration. In addition to apoptosis induction, this combined therapy also reduced the expression of several tumor-promoting factors including Fibroblast growth factors (FGF), vascular endothelial growth factor (VEGF), transforming growth factor-β (TGF-β), matrix metallopeptidases-2 (MMP-2), MMP-9, hypoxia-inducible factor-(HIF-1α), interleukin-6 (IL-6), IL-33, Bcl-x, vimentin, and snail.These findings indicate the potential of this nano-based anti-cancer therapeutic strategy for efficient cancer therapy which should be further investigated in future studies.
    Keywords angiogenesis ; apoptosis ; cancer therapy ; carcinogenesis ; cell movement ; enzymes ; fibroblast growth factors ; hypoxia-inducible factor 1 ; interleukin-6 ; nanoparticles ; neoplasm cells ; neoplasm progression ; neoplasms ; polyethylene ; signal transduction ; small interfering RNA ; transforming growth factor beta ; vascular endothelial growth factors ; vimentin
    Language English
    Dates of publication 2020-0515
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.117499
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    In stock of ZB MED Bonn / Germany

    Z 73/732: Show issues

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  3. Article: Blockade of CTLA-4 increases anti-tumor response inducing potential of dendritic cell vaccine

    Esmaily, Maryam / Masjedi, Ali / Hallaj, Shahin / Nabi Afjadi, Mohsen / Malakotikhah, Farinaz / Ghani, Sepideh / Ahmadi, Armin / Sojoodi, Mozhdeh / Hassannia, Hadi / Atyabi, Fatemeh / Namdar, Afshin / Azizi, Gholamreza / Ghalamfarsa, Ghasem / Jadidi-Niaragh, Farhad

    Journal of controlled release. 2020 Oct. 10, v. 326

    2020  

    Abstract: The immunosuppressive state of the tumor microenvironment diminishes the efficacy of dendritic cell (DC)-based cancer immunotherapy. Inhibitory immune checkpoint molecules expressed on tumor-infiltrating T lymphocytes, such as cytotoxic T-lymphocyte ... ...

    Abstract The immunosuppressive state of the tumor microenvironment diminishes the efficacy of dendritic cell (DC)-based cancer immunotherapy. Inhibitory immune checkpoint molecules expressed on tumor-infiltrating T lymphocytes, such as cytotoxic T-lymphocyte antigen 4 (CTLA-4) molecules are one of the main barriers in priming T cells by DCs. Therefore, it seems that blockade of such molecules facilitates the T cells activation by the DC vaccine. In this study, we intended to suppress the expression of CTLA-4 molecule on tumor-infiltrating T cells by siRNA-loaded chitosan-lactate (CL) nanoparticles to facilitate priming anti- tumor T cells by tumor lysate-loaded DC vaccine. Nanoparticles (NPs) have also provided an opportunity for specific drug delivery into the tumor site. CL NPs exhibited favorable physicochemical characteristics (size about 75 nm, polydispersive index<0.2, and a zeta potential about 14), which were associated with a high transfection rate and low toxicity. Moreover, the administration of anti-CTLA-4 siRNA-loaded NPs into CT26 and 4 T1 tumor -bearing mice led to the downregulation of CTLA-4 on tumor -infiltrating T cells, which was associated with tumor regression and increased mice survival.Moreover, while the treatment of tumor -bearing mice with DC vaccine had mild therapeutic outcomes, its combination with siRNA-loaded NPs may exhibit synergistic anti- tumor effects. This possible synergistic ameliorating effect is achieved through the reduction of immunosuppressive cells, the improved cytotoxicity of T lymphocytes, decreased inhibitory and increased inflammatory cytokines, and reduced angiogenesis and metastasis processes. These results indicate that the silencing of CTLA-4 can potentiate the T cell priming capacity of the DC vaccine, proposing a practical anti-cancer therapeutic approach.
    Keywords T-lymphocytes ; angiogenesis ; antigens ; cancer therapy ; cytokines ; cytotoxicity ; dendritic cells ; immunosuppression ; immunotherapy ; metastasis ; mice ; nanoparticles ; neoplasm cells ; neoplasms ; physicochemical properties ; remission ; transfection ; vaccines ; zeta potential
    Language English
    Dates of publication 2020-1010
    Size p. 63-74.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 632533-6
    ISSN 1873-4995 ; 0168-3659
    ISSN (online) 1873-4995
    ISSN 0168-3659
    DOI 10.1016/j.jconrel.2020.06.017
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2055: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Blockade of CTLA-4 increases anti-tumor response inducing potential of dendritic cell vaccine.

    Esmaily, Maryam / Masjedi, Ali / Hallaj, Shahin / Nabi Afjadi, Mohsen / Malakotikhah, Farinaz / Ghani, Sepideh / Ahmadi, Armin / Sojoodi, Mozhdeh / Hassannia, Hadi / Atyabi, Fatemeh / Namdar, Afshin / Azizi, Gholamreza / Ghalamfarsa, Ghasem / Jadidi-Niaragh, Farhad

    Journal of controlled release : official journal of the Controlled Release Society

    2020  Volume 326, Page(s) 63–74

    Abstract: The immunosuppressive state of the tumor microenvironment diminishes the efficacy of dendritic cell (DC)-based cancer immunotherapy. Inhibitory immune checkpoint molecules expressed on tumor-infiltrating T lymphocytes, such as cytotoxic T-lymphocyte ... ...

    Abstract The immunosuppressive state of the tumor microenvironment diminishes the efficacy of dendritic cell (DC)-based cancer immunotherapy. Inhibitory immune checkpoint molecules expressed on tumor-infiltrating T lymphocytes, such as cytotoxic T-lymphocyte antigen 4 (CTLA-4) molecules are one of the main barriers in priming T cells by DCs. Therefore, it seems that blockade of such molecules facilitates the T cells activation by the DC vaccine. In this study, we intended to suppress the expression of CTLA-4 molecule on tumor-infiltrating T cells by siRNA-loaded chitosan-lactate (CL) nanoparticles to facilitate priming anti- tumor T cells by tumor lysate-loaded DC vaccine. Nanoparticles (NPs) have also provided an opportunity for specific drug delivery into the tumor site. CL NPs exhibited favorable physicochemical characteristics (size about 75 nm, polydispersive index<0.2, and a zeta potential about 14), which were associated with a high transfection rate and low toxicity. Moreover, the administration of anti-CTLA-4 siRNA-loaded NPs into CT26 and 4 T1 tumor -bearing mice led to the downregulation of CTLA-4 on tumor -infiltrating T cells, which was associated with tumor regression and increased mice survival. Moreover, while the treatment of tumor -bearing mice with DC vaccine had mild therapeutic outcomes, its combination with siRNA-loaded NPs may exhibit synergistic anti- tumor effects. This possible synergistic ameliorating effect is achieved through the reduction of immunosuppressive cells, the improved cytotoxicity of T lymphocytes, decreased inhibitory and increased inflammatory cytokines, and reduced angiogenesis and metastasis processes. These results indicate that the silencing of CTLA-4 can potentiate the T cell priming capacity of the DC vaccine, proposing a practical anti-cancer therapeutic approach.
    MeSH term(s) Animals ; CTLA-4 Antigen/antagonists & inhibitors ; Cancer Vaccines ; Cell Line, Tumor ; Dendritic Cells ; Immunotherapy ; Mice ; Neoplasms/therapy
    Chemical Substances CTLA-4 Antigen ; Cancer Vaccines
    Language English
    Publishing date 2020-06-21
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632533-6
    ISSN 1873-4995 ; 0168-3659
    ISSN (online) 1873-4995
    ISSN 0168-3659
    DOI 10.1016/j.jconrel.2020.06.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2055: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Silencing of p68 and STAT3 synergistically diminishes cancer progression.

    Hashemi, Vida / Ahmadi, Armin / Malakotikhah, Farinaz / Chaleshtari, Mitra Ghasemi / Baghi Moornani, Mahdi / Masjedi, Ali / Sojoodi, Mozhdeh / Atyabi, Fatemeh / Nikkhoo, Afshin / Rostami, Narges / Baradaran, Behzad / Azizi, Gholamreza / Yousefi, Bahman / Ghalamfarsa, Ghasem / Jadidi-Niaragh, Farhad

    Life sciences

    2020  Volume 249, Page(s) 117499

    Abstract: Aims: Since several factors are involved in the tumorigenesis process, targeting only one factor most probably cannot overwhelm cancer progression. Therefore, it seems that combination therapy through targeting more than one cancer-related factor may ... ...

    Abstract Aims: Since several factors are involved in the tumorigenesis process, targeting only one factor most probably cannot overwhelm cancer progression. Therefore, it seems that combination therapy through targeting more than one cancer-related factor may lead to cancer control. The expression and function of p68 (DDX5; DEAD-Box Helicase 5) are dysregulated in various cancers. P68 is also a co-activator of many oncogenic transcription factors such as the signal transducer and activator of transcription-3 (STAT3), which contributes to cancer progression. This close connection between p68 and STAT3 plays an important role in the growth and development of cancer.
    Materials and methods: We decided to suppress the p68/STAT3 axis in various cancer cells by using Polyethylene glycol-trimethyl Chitosan-Hyaluronic acid (PEG-TMC-HA) nanoparticles (NPs) loaded with siRNA molecules. We assessed the impact of this combination therapy on apoptosis, proliferation, angiogenesis, and tumor growth, both in vitro and in vivo.
    Key findings: The results showed that siRNA-loaded NPs notably suppressed the expression of p68/STAT3 axis in cancer cells, which was associated with blockade of tumor growth, colony formation, angiogenesis, and cancer cell migration. In addition to apoptosis induction, this combined therapy also reduced the expression of several tumor-promoting factors including Fibroblast growth factors (FGF), vascular endothelial growth factor (VEGF), transforming growth factor-β (TGF-β), matrix metallopeptidases-2 (MMP-2), MMP-9, hypoxia-inducible factor-(HIF-1α), interleukin-6 (IL-6), IL-33, Bcl-x, vimentin, and snail.
    Significance: These findings indicate the potential of this nano-based anti-cancer therapeutic strategy for efficient cancer therapy which should be further investigated in future studies.
    MeSH term(s) Apoptosis ; Cell Line, Tumor ; Disease Progression ; Gene Silencing ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; STAT3 Transcription Factor/genetics ; eIF-2 Kinase/genetics
    Chemical Substances STAT3 Transcription Factor ; STAT3 protein, human ; eIF-2 Kinase (EC 2.7.11.1)
    Language English
    Publishing date 2020-03-03
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.117499
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.368: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Silencing adenosine A2a receptor enhances dendritic cell-based cancer immunotherapy.

    Masjedi, Ali / Ahmadi, Armin / Ghani, Sepideh / Malakotikhah, Farinaz / Nabi Afjadi, Mohsen / Irandoust, Mahzad / Karoon Kiani, Fariba / Heydarzadeh Asl, Sima / Atyabi, Fatemeh / Hassannia, Hadi / Hojjat-Farsangi, Mohammad / Namdar, Afshin / Ghalamfarsa, Ghasem / Jadidi-Niaragh, Farhad

    Nanomedicine : nanotechnology, biology, and medicine

    2020  Volume 29, Page(s) 102240

    Abstract: Overexpression of adenosine in the tumor region leads to suppression of various immune cells, particularly T cells through ligation with adenosine 2a receptor (A2aR). In this study, we intended to increase the efficacy of tumor lysate-loaded DC vaccine ... ...

    Abstract Overexpression of adenosine in the tumor region leads to suppression of various immune cells, particularly T cells through ligation with adenosine 2a receptor (A2aR). In this study, we intended to increase the efficacy of tumor lysate-loaded DC vaccine by silencing the expression of A2aR on T cells through the application of A2aR-specific siRNA-loaded PEG-chitosan-lactate (PCL) nanoparticles (NPs) in the 4T1 breast tumor-bearing mice. Combination therapy by DC vaccine and siRNA-loaded NPs markedly induced tumor regression and increased survival time of mice. These ameliorative effects were partly via downregulation of immunosuppressive cells, increased function of cytotoxic T lymphocytes, and induction of immune-stimulatory cytokines. Moreover, combination therapy could markedly suppress angiogenesis and metastasis processes. These results imply the efficacy of novel combination therapy for the treatment of breast cancer by using A2aR siRNA-loaded NPs and DC vaccine which can be translated into the initial phase of clinical trials in the near future.
    MeSH term(s) Adenosine A2 Receptor Antagonists/chemistry ; Adenosine A2 Receptor Antagonists/pharmacology ; Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/immunology ; Breast Neoplasms/pathology ; Breast Neoplasms/therapy ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; Cancer Vaccines/pharmacology ; Cell Line, Tumor ; Chitosan/chemistry ; Chitosan/pharmacology ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Disease Models, Animal ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Immunotherapy ; Lactic Acid/chemistry ; Lactic Acid/pharmacology ; Mammary Neoplasms, Animal/genetics ; Mammary Neoplasms, Animal/pathology ; Mammary Neoplasms, Animal/therapy ; Mice ; Nanoparticles/chemistry ; Polyethylene Glycols/chemistry ; Polyethylene Glycols/pharmacology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/pharmacology ; Receptor, Adenosine A2A/genetics ; T-Lymphocytes, Cytotoxic/drug effects ; T-Lymphocytes, Cytotoxic/immunology
    Chemical Substances Adenosine A2 Receptor Antagonists ; Cancer Vaccines ; RNA, Small Interfering ; Receptor, Adenosine A2A ; Lactic Acid (33X04XA5AT) ; Polyethylene Glycols (3WJQ0SDW1A) ; Chitosan (9012-76-4)
    Language English
    Publishing date 2020-06-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2183417-9
    ISSN 1549-9642 ; 1549-9634
    ISSN (online) 1549-9642
    ISSN 1549-9634
    DOI 10.1016/j.nano.2020.102240
    Database MEDical Literature Analysis and Retrieval System OnLINE

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