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Monoclonal Antibody Therapy and Colony- Stimulating Factor in Treating Patients With Metastatic Colorectal Cancer

ABSTRACT: RATIONALE: Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. Colony-stimulating factors such as G-CSF may increase the number of immune cells found in bone marrow or peripheral blood, and may help a person’s immune system kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of monoclonal antibody therapy plus G-CSF in treating patients with metastatic colorectal cancer that has not responded to treatment with fluorouracil.

DISEASE(S): Colorectal Cancer,Colorectal Neoplasms

PROVIDER: 2002323 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Vaccine Therapy and GM-CSF in Treating Patients With CNS Lymphoma

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Rebeccamycin Analog and Cisplatin With or Without Filgrastim in Treating Patients With Advanced Cancer

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GM-CSF and Combination Chemotherapy in Treating Patients Who Are Undergoing Surgery for Stage II or Stage III Colon Cancer

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Adrianne2018 - Modelling combined virotherapy and immunotherapy: strengthening the antitumour immune response mediated by IL-12 and GM-CSF expression

Project description:Modelling combined virotherapy and immunotherapy:strengthening the antitumour immune response mediated byIL-12 and GM-CSF expression Adrianne L. Jennera, Chae-Ok Yunb, Arum Yoonb, Adelle C. F. Costercand Peter S. Kimaa School of Mathematics and Statistics, University of Sydney, Sydney, Australia;bDepartment ofBioengineering, Hanyang University, Seoul, Korea;cSchool of Mathematics and Statistics, University of NewSouth Wales, Sydney, Australia ABSTRACT Combined virotherapy and immunotherapy has been emergingas a promising and effective cancer treatment for some time.Intratumoural injections of an oncolytic virus instigate an immunereaction in the host, resulting in an influx of immune cells tothe tumour site. Through combining an oncolytic viral vector withimmunostimulatory cytokines an additional antitumour immuneresponse can be initiated, whereby immune cells induce apoptosisin both uninfected and virus infected tumour cells. We developa mathematical model to reproduce the experimental results fortumour growth under treatment with an oncolytic adenovirus co-expressing the immunostimulatory cytokines interleukin 12 (IL-12)and granulocyte-monocyte colony stimulating factor (GM-CSF). Byexploring heterogeneity in the immune cell stimulation by thetreatment, we find a subset of the parameter space for the immunecell induced apoptosis rate, in which the treatment will be lesseffective in a short time period. Therefore, we believe the bivariatenature of treatment outcome, whereby tumours are either completelyeradicated or grow unbounded, can be explained by heterogeneity inthis immune characteristic. Furthermore, the model highlights theapparent presence of negative feedback in the helper T cell and APCstimulation dynamics, when IL-12 and GM-CSF are co-expressed asopposed to individually expressed by the viral vector.

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RNA-seq analysis of αPD-1 treatment outcomes in IL-34 expressing or not expressing CT26 cell line

Project description:Interleukin-34 (IL-34) is an alternative ligand to colony-stimulating factor-1 (CSF-1) for the CSF-1 receptor that acts as a key regulator of monocyte/macrophage lineage. In this study, we show that cancer cells-derived IL-34 mediates resistance to immune checkpoint blockade regardless of CSF-1 existence. In a therapeutic study of a programmed death-1 and cytotoxic T-lymphocyte-associated antigen-4 blocking monoclonal antibody, the expression of IL-34 in tumors was accompanied with limited benefits compared to IL-34 non-expressing tumors in various murine cancer models. Consistent with its immunosuppressive characteristics, the expression of IL-34 in tumors correlates with decreased frequencies of cellular (such as CD8+ and CD4+ T cells) and molecular (including various cytokines and chemokines) effectors at the tumor microenvironment. In addition, IL-34 blockade expands the M1-macrophage population. Then, a neutralizing antibody against IL-34 helped to reverse these effects and improved the therapeutic effects of the immune checkpoint blockade in combinatorial therapeutic models, including a patient-derived xenograft model of primary lung adenocarcinoma. Collectively, we revealed that tumor-derived IL-34 inhibits the efficacy of immune checkpoint blockade and proposed the utility of IL-34 blockade as a new strategy for cancer therapy.

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