LIVIVO - Search results -

Search results

Result 1 - 10 of total 30

Search options

Article ; Online: Replication and Spread of Oncolytic Herpes Simplex Virus in Solid Tumors.

Hong, Bangxing / Sahu, Upasana / Mullarkey, Matthew P / Kaur, Balveen

2022 Volume 14, Issue 1

Abstract: Oncolytic herpes simplex virus (oHSV) is a highly promising treatment for solid tumors. Intense research and development efforts have led to first-in-class approval for an oHSV for melanoma, but barriers to this promising therapy still exist that limit ... ...

Abstract	Oncolytic herpes simplex virus (oHSV) is a highly promising treatment for solid tumors. Intense research and development efforts have led to first-in-class approval for an oHSV for melanoma, but barriers to this promising therapy still exist that limit efficacy. The process of infection, replication and transmission of oHSV in solid tumors is key to obtaining a good lytic destruction of infected cancer cells to kill tumor cells and release tumor antigens that can prime anti-tumor efficacy. Intracellular tumor cell signaling and tumor stromal cells present multiple barriers that resist oHSV activity. Here, we provide a review focused on oncolytic HSV and the essential viral genes that allow for virus replication and spread in order to gain insight into how manipulation of these pathways can be exploited to potentiate oHSV infection and replication among tumor cells.
MeSH term(s)	Animals ; Cell Line, Tumor ; Herpes Simplex ; Herpesvirus 1, Human/genetics ; Humans ; Neoplasms/therapy ; Oncolytic Virotherapy ; Oncolytic Viruses/genetics ; Tropism ; Virus Replication
Language	English
Publishing date	2022-01-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14010118
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article: oHSV-P10 reduces glioma stem cell enrichment after oncolytic HSV therapy.

Sahu, Upasana / Mullarkey, Matthew P / Pei, Guangsheng / Zhao, Zhongming / Hong, Bangxing / Kaur, Balveen

Molecular therapy oncolytics

2023 Volume 29, Page(s) 30–41

Abstract: Longstanding evidence implicate glioma stem-like cells as the main drivers contributing toward glioblastoma (GBM) therapy resistance and tumor recurrence. Although oncolytic herpes simplex virus (oHSV) viral therapy is a promising biological therapy ... ...

Abstract	Longstanding evidence implicate glioma stem-like cells as the main drivers contributing toward glioblastoma (GBM) therapy resistance and tumor recurrence. Although oncolytic herpes simplex virus (oHSV) viral therapy is a promising biological therapy recently approved for melanoma (in the United States and Europe) and GBM (in Japan); however, the impact of this therapy on GBM stem-like cells (GSCs) is understudied. Here we show that post-oHSV virotherapy activated AKT signaling results in an enrichment of GSC signatures in glioma, which mimics the enrichment in GSC observed after radiation treatment. We also uncovered that a second-generation oncolytic virus armed with PTEN-L (oHSV-P10) decreases this by moderating IL6/JAK/STAT3 signaling. This ability was retained in the presence of radiation treatment and oHSV-P10-sensitized intracranial GBM to radiotherapy. Collectively, our findings uncover potential mechanisms to overcome GSC-mediated radiation resistance via oHSV-P10.
Language	English
Publishing date	2023-04-03
Publishing country	United States
Document type	Journal Article
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2023.03.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Replication and Spread of Oncolytic Herpes Simplex Virus in Solid Tumors

Hong, Bangxing / Sahu, Upasana / Mullarkey, Matthew P. / Kaur, Balveen

Viruses. 2022 Jan. 10, v. 14, no. 1

2022

Abstract	Oncolytic herpes simplex virus (oHSV) is a highly promising treatment for solid tumors. Intense research and development efforts have led to first-in-class approval for an oHSV for melanoma, but barriers to this promising therapy still exist that limit efficacy. The process of infection, replication and transmission of oHSV in solid tumors is key to obtaining a good lytic destruction of infected cancer cells to kill tumor cells and release tumor antigens that can prime anti-tumor efficacy. Intracellular tumor cell signaling and tumor stromal cells present multiple barriers that resist oHSV activity. Here, we provide a review focused on oncolytic HSV and the essential viral genes that allow for virus replication and spread in order to gain insight into how manipulation of these pathways can be exploited to potentiate oHSV infection and replication among tumor cells.
Keywords	herpes simplex ; melanoma ; neoplasm cells ; research and development ; therapeutics ; virus replication ; viruses
Language	English
Dates of publication	2022-0110
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v14010118
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: PKR induces TGF-β and limits oncolytic immune therapy.

Hong, Bangxing / Sahu, Upasana / Mullarkey, Matthew P / Hong, Evan / Pei, Guangsheng / Yan, Yuanqing / Otani, Yoshihiro / Banasavadi-Siddegowda, Yeshavanth / Fan, Huihui / Zhao, Zhongming / Yu, Jianhua / Caligiuri, Michael A / Kaur, Balveen

Journal for immunotherapy of cancer

2023 Volume 11, Issue 2

Abstract: Background: Mammalian cells have developed multiple intracellular mechanisms to defend against viral infections. These include RNA-activated protein kinase (PKR), cyclic GMP-AMP synthase and stimulation of interferon genes (cGAS-STING) and toll-like ... ...

Abstract	Background: Mammalian cells have developed multiple intracellular mechanisms to defend against viral infections. These include RNA-activated protein kinase (PKR), cyclic GMP-AMP synthase and stimulation of interferon genes (cGAS-STING) and toll-like receptor-myeloid differentiation primary response 88 (TLR-MyD88). Among these, we identified that PKR presents the most formidable barrier to oncolytic herpes simplex virus (oHSV) replication in vitro. Methods: To elucidate the impact of PKR on host responses to oncolytic therapy, we generated a novel oncolytic virus (oHSV-shPKR) which disables tumor intrinsic PKR signaling in infected tumor cells. Results: As anticipated, oHSV-shPKR resulted in suppression of innate antiviral immunity and improves virus spread and tumor cell lysis both in vitro and in vivo. Single cell RNA sequencing combined with cell-cell communication analysis uncovered a strong correlation between PKR activation and transforming growth factor beta (TGF-ß) immune suppressive signaling in both human and preclinical models. Using a murine PKR targeting oHSV, we found that in immune-competent mice this virus could rewire the tumor immune microenvironment to increase the activation of antigen presentation and enhance tumor antigen-specific CD8 T cell expansion and activity. Further, a single intratumoral injection of oHSV-shPKR significantly improved the survival of mice bearing orthotopic glioblastoma. To our knowledge, this is the first report to identify dual and opposing roles of PKR wherein PKR activates antivirus innate immunity and induces TGF-ß signaling to inhibit antitumor adaptive immune responses. Conclusions: Thus, PKR represents the Achilles heel of oHSV therapy, restricting both viral replication and antitumor immunity, and an oncolytic virus that can target this pathway significantly improves response to virotherapy.
MeSH term(s)	Animals ; Humans ; Mice ; Brain Neoplasms/pathology ; Oncolytic Virotherapy/methods ; Oncolytic Viruses ; Simplexvirus ; Transforming Growth Factor beta ; Tumor Microenvironment ; eIF-2 Kinase/metabolism
Chemical Substances	Transforming Growth Factor beta ; eIF-2 Kinase (EC 2.7.11.1)
Language	English
Publishing date	2023-02-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2022-006164
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: esRAGE-expressing oHSV enhances anti-tumor efficacy by inhibition of endothelial cell activation.

Swanner, Jessica / Shim, Ji Seon / Rivera-Caraballo, Kimberly A / Vázquez-Arreguín, Karina / Hong, Bangxing / Bueso-Perez, Alberto J / Lee, Tae Jin / Banasavadi-Siddegowda, Yeshavanth Kumar / Kaur, Balveen / Yoo, Ji Young

Molecular therapy oncolytics

2023 Volume 28, Page(s) 171–181

Abstract: High-mobility group box 1 (HMGB1) is a damage-associated molecular pattern (DAMP) molecule that plays an important role in inflammation and tumorigenesis. Receptor for advanced glycation end products (RAGE) is one of the major receptors to which ... ...

Abstract	High-mobility group box 1 (HMGB1) is a damage-associated molecular pattern (DAMP) molecule that plays an important role in inflammation and tumorigenesis. Receptor for advanced glycation end products (RAGE) is one of the major receptors to which extracellular HMGB1 binds to mediate its activity. RAGE is highly expressed on the endothelial cells (ECs) and regulates endothelial permeability during inflammation. Here, we introduced the endogenous secretory form of RAGE (esRAGE) as a decoy receptor for RAGE ligands into an oncolytic herpes simplex virus 1 (oHSV) (OVesRAGE), which, upon release, can function to block RAGE signaling. OVesRAGE significantly decreased phosphorylation of MEK1/2 and Erk and increased cleaved PARP in glioblastoma (GBM) cells
Language	English
Publishing date	2023-01-16
Publishing country	United States
Document type	Journal Article
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2023.01.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: HOX and PBX gene dysregulation as a therapeutic target in glioblastoma multiforme.

Arunachalam, Einthavy / Rogers, William / Simpson, Guy R / Möller-Levet, Carla / Bolton, Gemma / Ismael, Mohammed / Smith, Christopher / Keegen, Karl / Bagwan, Izhar / Brend, Tim / Short, Susan C / Hong, Bangxing / Otani, Yoshihiro / Kaur, Balveen / Annels, Nicola / Morgan, Richard / Pandha, Hardev

BMC cancer

2022 Volume 22, Issue 1, Page(s) 400

Abstract: Background: Glioblastoma multiforme (GBM) is the most common high-grade malignant brain tumour in adults and arises from the glial cells in the brain. The prognosis of treated GBM remains very poor with 5-year survival rates of 5%, a figure which has ... ...

Abstract	Background: Glioblastoma multiforme (GBM) is the most common high-grade malignant brain tumour in adults and arises from the glial cells in the brain. The prognosis of treated GBM remains very poor with 5-year survival rates of 5%, a figure which has not improved over the last few decades. Currently, there is a modest 14-month overall median survival in patients undergoing maximum safe resection plus adjuvant chemoradiotherapy. HOX gene dysregulation is now a widely recognised feature of many malignancies. Methods: In this study we have focused on HOX gene dysregulation in GBM as a potential therapeutic target in a disease with high unmet need. Results: We show significant dysregulation of these developmentally crucial genes and specifically that HOX genes A9, A10, C4 and D9 are strong candidates for biomarkers and treatment targets for GBM and GBM cancer stem cells. We evaluated a next generation therapeutic peptide, HTL-001, capable of targeting HOX gene over-expression in GBM by disrupting the interaction between HOX proteins and their co-factor, PBX. HTL-001 induced both caspase-dependent and -independent apoptosis in GBM cell lines. Conclusion: In vivo biodistribution studies confirmed that the peptide was able to cross the blood brain barrier. Systemic delivery of HTL-001 resulted in improved control of subcutaneous murine and human xenograft tumours and improved survival in a murine orthotopic model.
MeSH term(s)	Adult ; Animals ; Brain Neoplasms/drug therapy ; Brain Neoplasms/genetics ; Cell Line, Tumor ; Genes, Homeobox ; Glioblastoma/drug therapy ; Glioblastoma/therapy ; Humans ; Mice ; Peptides/genetics ; Tissue Distribution
Chemical Substances	Peptides
Language	English
Publishing date	2022-04-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2041352-X
ISSN	1471-2407 ; 1471-2407
ISSN (online)	1471-2407
ISSN	1471-2407
DOI	10.1186/s12885-022-09466-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Engineering Oncolytic Vaccinia Virus to redirect Macrophages to Tumor Cells.

Cao, Felicia / Nguyen, Phuong / Hong, Bangxing / DeRenzo, Christopher / Rainusso, Nino C / Rodriguez Cruz, Tania / Wu, Meng-Fen / Liu, Hao / Song, Xiao-Tong / Suzuki, Masataka / Wang, Lisa L / Yustein, Jason T / Gottschalk, Stephen

Advances in cell and gene therapy

2020 Volume 4, Issue 2

Abstract: Oncolytic virotherapy has been tested in numerous early phase clinical studies. However, the antitumor activity of oncolytic viruses thus far has been limited. Numerous strategies are being explored to enhance their antitumor activity by activating the ... ...

Abstract	Oncolytic virotherapy has been tested in numerous early phase clinical studies. However, the antitumor activity of oncolytic viruses thus far has been limited. Numerous strategies are being explored to enhance their antitumor activity by activating the adaptive arm of the immune system. We reasoned that it might also be possible to engineer oncolytic viruses to redirect tumor-associated macrophages to tumor cells for therapeutic benefit. We engineered an oncolytic vaccinia virus (VV) to disrupt the CD47/SIRPα interaction by expressing a chimeric molecule that consists of the ectodomain of SIRPα and the Fc domain of IgG4 (SIRPα-Fc-VV). SIRPα-Fc-VV readily replicated in tumor cells and redirected M1 as well as M2 macrophages to tumor cells
Language	English
Publishing date	2020-07-03
Publishing country	United States
Document type	Journal Article
ISSN	2573-8461
ISSN (online)	2573-8461
DOI	10.1002/acg2.99
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: Oncolytic HSV Therapy Modulates Vesicular Trafficking Inducing Cisplatin Sensitivity and Antitumor Immunity.

Hong, Bangxing / Chapa, Valerie / Saini, Uksha / Modgil, Puneet / Cohn, David E / He, Guangan / Siddik, Zahid H / Sood, Anil K / Yan, Yuanqing / Selvendiran, Karuppaiyah / Pei, Guangsheng / Zhao, Zhongming / Yoo, Ji Young / Kaur, Balveen

Clinical cancer research : an official journal of the American Association for Cancer Research

2020 Volume 27, Issue 2, Page(s) 542–553

Abstract: Purpose: Here we investigated the impact of oncolytic herpes simplex virus (HSV) treatment on cisplatin sensitivity of platinum-resistant ovarian cancer, and the impact of the combination on immunotherapy.: Experimental design: Therapeutic efficacy ... ...

Abstract	Purpose: Here we investigated the impact of oncolytic herpes simplex virus (HSV) treatment on cisplatin sensitivity of platinum-resistant ovarian cancer, and the impact of the combination on immunotherapy. Experimental design: Therapeutic efficacy of the combination was assessed in platinum-resistant human and murine ovarian cancer peritoneal metastatic mouse models ( Results: Gene Ontology pathway analysis uncovered disruption of cellular extracellular vesicle (EV)-related pathways in infected cells (FDR = 2.97E-57). Mechanistically, we identified reduced expression of transporters expressed on EV implicated in cisplatin efflux. The increased cisplatin retention led to increased cisplatin-DNA adducts, which resulted in micronuclei and the subsequent activation of cGAS-STING pathway with a significant activation of innate immune cells and translated to an increase in antitumor immunity and efficacy. In mice bearing platinum-resistant ovarian cancer, we also observed a feedback induction of PD-L1 on tumor cells, which sensitized combination-treated mice to anti-PD-1 immune checkpoint therapy. Conclusions: To our knowledge, this is the first report to show HSV-induced cisplatin retention in infected cells. The consequential increased damaged DNA was then expelled from cells as micronuclei which resulted in induction of inflammatory responses and education of antitumor immunity. The combination therapy also created an environment that sensitized tumors to immune checkpoint therapy.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Cells, Cultured ; Cisplatin/therapeutic use ; Combined Modality Therapy ; DNA Adducts/genetics ; DNA Adducts/immunology ; Disease Models, Animal ; Female ; Herpesvirus 1, Human/physiology ; Humans ; Immunotherapy/methods ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Oncolytic Virotherapy/methods ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/therapy ; Ovarian Neoplasms/virology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Treatment Outcome ; Xenograft Model Antitumor Assays/methods ; Mice
Chemical Substances	Antineoplastic Agents ; DNA Adducts ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2020-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-20-2210
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4223: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: NOTCH-Induced MDSC Recruitment after oHSV Virotherapy in CNS Cancer Models Modulates Antitumor Immunotherapy.

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 Volume 28, Issue 7, Page(s) 1460–1473

Abstract: Purpose: Oncolytic herpes simplex virus-1 (oHSV) infection of brain tumors activates NOTCH, however the consequences of NOTCH on oHSV-induced immunotherapy is largely unknown. Here we evaluated the impact of NOTCH blockade on virus-induced immunotherapy. ...

Abstract	Purpose: Oncolytic herpes simplex virus-1 (oHSV) infection of brain tumors activates NOTCH, however the consequences of NOTCH on oHSV-induced immunotherapy is largely unknown. Here we evaluated the impact of NOTCH blockade on virus-induced immunotherapy. Experimental design: RNA sequencing (RNA-seq), TCGA data analysis, flow cytometry, Luminex- and ELISA-based assays, brain tumor animal models, and serum analysis of patients with recurrent glioblastoma (GBM) treated with oHSV was used to evaluate the effect of NOTCH signaling on virus-induced immunotherapy. Results: TCGA data analysis of patients with grade IV glioma and oHSV treatment of experimental brain tumors in mice showed that NOTCH signaling significantly correlated with a higher myeloid cell infiltration. Immunofluorescence staining and RNA-seq uncovered a significant induction of Jag1 (NOTCH ligand) expression in infiltrating myeloid cells upon oHSV infection. Jag1-expressing macrophages further spread NOTCH activation in the tumor microenvironment (TME). NOTCH-activated macrophages increased the secretion of CCL2, which further amplified myeloid-derived suppressor cells. CCL2 and IL10 induction was also observed in serum of patients with recurrent GBM treated with oHSV (rQnestin34.5; NCT03152318). Pharmacologic blockade of NOTCH signaling rescued the oHSV-induced immunosuppressive TME and activated a CD8-dependent antitumor memory response, resulting in a therapeutic benefit. Conclusions: NOTCH-induced immunosuppressive myeloid cell recruitment limited antitumor immunity. Translationally, these findings support the use of NOTCH inhibition in conjunction with oHSV therapy.
MeSH term(s)	Animals ; Cell Line, Tumor ; Glioblastoma/pathology ; Humans ; Immunotherapy ; Mice ; Myeloid-Derived Suppressor Cells/metabolism ; Neoplasm Recurrence, Local/therapy ; Oncolytic Virotherapy/methods ; Oncolytic Viruses/genetics ; Simplexvirus ; Tumor Microenvironment ; Xenograft Model Antitumor Assays
Language	English
Publishing date	2022-01-12
Publishing country	United States
Document type	Clinical Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-2347
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4223: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: USP18 is crucial for IFN-γ-mediated inhibition of B16 melanoma tumorigenesis and antitumor immunity.

Hong, Bangxing / Li, Haiyan / Lu, Yong / Zhang, Mingjun / Zheng, Yuhuan / Qian, Jianfei / Yi, Qing

Molecular cancer

2014 Volume 13, Page(s) 132

Abstract: Background: Interferon (IFN)-γ-mediated immune response plays an important role in tumor immunosurveillance. However, the regulation of IFN-γ-mediated tumorigenesis and immune response remains elusive. USP18, an interferon stimulating response element, ... ...

Abstract	Background: Interferon (IFN)-γ-mediated immune response plays an important role in tumor immunosurveillance. However, the regulation of IFN-γ-mediated tumorigenesis and immune response remains elusive. USP18, an interferon stimulating response element, regulates IFN-α-mediated signaling in anti-viral immune response, but its role in IFN-γ-mediated tumorigenesis and anti-tumor immune response is unknown. Method: In this study, USP18 in tumorigenesis and anti-tumor immune response was comprehensively appraised in vivo by overexpression or downregulation its expression in murine B16 melanoma tumor model in immunocompetent and immunodeficient mice. Results: Ectopic expression or downregulation of USP18 in B16 melanoma tumor cells inhibited or promoted tumorigenesis, respectively, in immunocompetent mice. USP18 expression in B16 melanoma tumor cells regulated IFN-γ-mediated immunoediting, including upregulating MHC class-I expression, reducing tumor cell-mediated inhibition of T cell proliferation and activation, and suppressing PD-1 expression in CD4+ and CD8+ T cells in tumor-bearing mice. USP18 expression in B16 melanoma tumor cells also enhanced CTL activity during adoptive immunotherapy by prolonging the persistence and enhancing the activity of adoptively transferred CTLs and by reducing CTL exhaustion in the tumor microenvironment. Mechanistic studies demonstrated that USP18 suppressed tumor cell-mediated immune inhibition by activating T cells, inhibiting T-cell exhaustion, and reducing dendritic cell tolerance, thus sensitizing tumor cells to immunosurveillance and immunotherapy. Conclusion: These findings suggest that stimulating USP18 is a feasible approach to induce B16 melanoma specific immune response.
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/pathology ; Carcinogenesis/genetics ; Carcinogenesis/immunology ; Carcinogenesis/pathology ; Cell Proliferation ; Cytotoxicity, Immunologic ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Female ; Gene Expression Regulation, Neoplastic/immunology ; Histocompatibility Antigens Class I/genetics ; Histocompatibility Antigens Class I/immunology ; Immunity, Innate ; Immunotherapy, Adoptive ; Interferon-gamma/genetics ; Interferon-gamma/immunology ; Melanoma, Experimental/genetics ; Melanoma, Experimental/immunology ; Melanoma, Experimental/pathology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Neoplasm Transplantation ; Programmed Cell Death 1 Receptor/genetics ; Programmed Cell Death 1 Receptor/immunology ; Signal Transduction ; Skin Neoplasms/genetics ; Skin Neoplasms/immunology ; Skin Neoplasms/pathology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/pathology ; T-Lymphocytes, Cytotoxic/transplantation ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/immunology
Chemical Substances	Histocompatibility Antigens Class I ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Interferon-gamma (82115-62-6) ; Usp18 protein, mouse (EC 3.4.19.-) ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2014-05-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/1476-4598-13-132
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED