Glutamine Antagonist Synergizes with Electrodynamic Therapy to Induce Tumor Regression and Systemic Antitumor Immunity

ACS Nano ◽  
2022 ◽  
Author(s):  
Gui Chen ◽  
Qing Xu ◽  
Zhenzhen Feng ◽  
Qinqin Xu ◽  
Xuhui Zhang ◽  
...  
Keyword(s):  
Antitumor Immunity ◽  
Tumor Regression ◽  
Induce Tumor Regression

Radioimmunotherapy of Xenografts of Human Pancreatic Carcinomas - Intravenous and Intratumoral Application of 131l-Labelled Monoclonal Antibodies

1986 ◽  
Vol 25 (06) ◽  
pp. 235-238 ◽  
Author(s):  
S. Lander ◽  
M. Bahlo ◽  
R. Montz ◽  
R. Klapdor
Keyword(s):  
Irradiation Dose ◽  
Tumor Regression ◽  
Whole Body ◽  
Inhibit Tumor Growth ◽  
Local Irradiation ◽  
Clinical Value ◽  
Direct Radiation ◽  
Intravenous Injections ◽  
Induce Tumor Regression ◽  
High Doses

The effects of radioimmunotherapy were tested in xenografts of 2 different human pancreatic carcinomas comparing the intravenous and intratumoral application. On principle, intravenous injections of high doses of 131l-anti- Ca 19-9 or -BW 494/32 may inhibit tumor growth. In view of the low direct radiation dose (360-2100 rad), however, other factors than direct toxic effects have to be discussed, e. g. systemic effects due to the high whole-body irradiation. Intratumoral application, however, may induce tumor regression or growth inhibition due to the high local irradiation dose. Consequently, this treatment modality might be of clinical value at least in some patients.

scholarly journals Cabozantinib and dasatinib synergize to induce tumor regression in non-clear cell renal cell carcinoma

2021 ◽  
pp. 100267
Author(s):  
Hui-wen Lue ◽  
Daniel S. Derrick ◽  
Soumya Rao ◽  
Ahna Van Gaest ◽  
Larry Cheng ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Tumor Regression ◽  
Cell Renal Cell Carcinoma ◽  
Induce Tumor Regression

scholarly journals TLR4/IFNγ pathways induce tumor regression via NOS II-dependent NO and ROS production in murine breast cancer models

2015 ◽  
Vol 5 (5) ◽  
pp. e1123369 ◽  
Author(s):  
Myriam Lamrani ◽  
Nejia Sassi ◽  
Catherine Paul ◽  
Nadhir Yousfi ◽  
Jean-Luc Boucher ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Regression ◽  
Ros Production ◽  
Induce Tumor Regression ◽  
Cancer Models

Fusion Hybrid of Dendritic Cells and Engineered Tumor Cells Expressing Interleukin-12 Induces Type 1 Immune Responses against Tumor

2005 ◽  
Vol 91 (6) ◽  
pp. 531-538 ◽  
Author(s):  
Meiqing Shi ◽  
Liping Su ◽  
Sigou Hao ◽  
Xulin Guo ◽  
Jim Xiang
Keyword(s):  
Cancer Immunotherapy ◽  
Tumor Cells ◽  
Antitumor Immunity ◽  
Cytotoxic T Lymphocyte ◽  
Tumor Regression ◽  
Interleukin 12 ◽  
Myeloma Cells ◽  
Th1 Cytokine

Aims and Background Dendritic cell (DC)-tumor fusion hybrid vaccinees that facilitate antigen presentation represent a novel powerful strategy in cancer immunotherapy. Preclinical studies have demonstrated that IL-12 promotes specific antitumor immunity mediated by T cells in several types of tumors. In the present study, we investigated the antitumor immunity derived from vaccination of fusion hybrids between DCs and engineered J558/IL-12 myeloma cells secreting Th1 cytokine IL-12. Methods The expression vector pcDNA-IL-12 was generated and transfected into J558 myeloma cells and then bone marrow-derived DCs were fused with engineered J558/IL-12 cells. The antitumor immunity derived from vaccination of the fusion hybrid DC/J558/IL-12 was evaluated in vitro and in vivo. Results DC/J558/IL-12 cells secreted recombinant IL-12 (1.6 ng/mL), and inoculation of BALB/c mice with DC/J558/IL-12 hybrid induced a Th1 dominant immune response and resulted in tumor regression. Immunization of mice with engineered DC/J558/IL-12 hybrid elicited stronger J558 tumor-specific cytotoxic T lymphocyte (CTL) responses in vitro as well as more potent protective immunity against J558 tumor challenge in vivo than immunization with the mixture of DCs and J558/IL-12, J558/IL-12 and J558, respectively. Furthermore, the antitumor immunity mediated by DC/J558/1L-12 tumor cell vaccination in vivo appeared to be dependent on CD8+ CTL. Conclusions These results demonstrate that the engineered fusion hybrid vaccines that combine Th1 cytokine gene-modified tumor cells with DCs may be an attractive strategy for cancer immunotherapy.

CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma

2013 ◽  
Vol 12 (7) ◽  
pp. 1171-1179 ◽  
Author(s):  
Roberto A. Salas Fragomeni ◽  
Hye Won Chung ◽  
Yosef Landesman ◽  
William Senapedis ◽  
Jean-Richard Saint-Martin ◽  
...  
Keyword(s):  
Tumor Regression ◽  
Induce Tumor Regression ◽  
Braf Inhibition ◽  
Braf Mutant

scholarly journals Combination Therapy with Local Radiofrequency Ablation and Systemic Vaccine Enhances Antitumor Immunity and Mediates Local and Distal Tumor Regression

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e70417 ◽  
Author(s):  
Sofia R. Gameiro ◽  
Jack P. Higgins ◽  
Matthew R. Dreher ◽  
David L. Woods ◽  
Goutham Reddy ◽  
...  
Keyword(s):  
Radiofrequency Ablation ◽  
Combination Therapy ◽  
Antitumor Immunity ◽  
Tumor Regression ◽  
Distal Tumor

scholarly journals Specific targeting of CD163+ TAMs mobilizes inflammatory monocytes and promotes T cell–mediated tumor regression

2019 ◽  
Vol 216 (10) ◽  
pp. 2394-2411 ◽  
Author(s):  
Anders Etzerodt ◽  
Kyriaki Tsalkitzi ◽  
Maciej Maniecki ◽  
William Damsky ◽  
Marcello Delfini ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tumor Progression ◽  
Antitumor Immunity ◽  
Tumor Regression ◽  
Human Cancer ◽  
Experimental Models ◽  
Activated T Cells ◽  
Specific Targeting ◽  
Inflammatory Monocytes

Tumor-associated macrophages (TAMs) play critical roles in tumor progression but are also capable of contributing to antitumor immunity. Recent studies have revealed an unprecedented heterogeneity among TAMs in both human cancer and experimental models. Nevertheless, we still understand little about the contribution of different TAM subsets to tumor progression. Here, we demonstrate that CD163-expressing TAMs specifically maintain immune suppression in an experimental model of melanoma that is resistant to anti–PD-1 checkpoint therapy. Specific depletion of the CD163+ macrophages results in a massive infiltration of activated T cells and tumor regression. Importantly, the infiltration of cytotoxic T cells was accompanied by the mobilization of inflammatory monocytes that significantly contributed to tumor regression. Thus, the specific targeting of CD163+ TAMs reeducates the tumor immune microenvironment and promotes both myeloid and T cell–mediated antitumor immunity, illustrating the importance of selective targeting of tumor-associated myeloid cells in a therapeutic context.

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