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

ABSTRACT: RATIONALE: Vaccines made from a person’s cancer proteins may help the body build an effective immune response to kill cancer cells. Colony-stimulating factors, such as GM-CSF, may increase the number of immune cells found in bone marrow or peripheral blood. Giving vaccine therapy together with GM-CSF may make a stronger immune response and kill more cancer cells. PURPOSE: This phase II trial is studying the side effects and how well giving vaccine therapy together with GM-CSF works in treating patients with CNS lymphoma.

DISEASE(S): Lymphoproliferative Disorders,Central Nervous System Neoplasms,Lymphoproliferative Disorder,Nervous System Neoplasms,Small Intestine Cancer,Angioimmunoblastic T-cell Lymphoma,Brain And Central Nervous System Tumors,Intestinal Neoplasms,Lymphoma

PROVIDER: 2051068 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Vaccine Therapy in Treating Patients With Liver or Lung Metastases From Colorectal Cancer

Project description:RATIONALE: Vaccines made from a gene-modified virus and a person’s white blood cells may make the body build an effective immune response to kill tumor cells. Biological therapies, such as Granulocyte-macrophage colony-stimulating factor (GM-CSF), may stimulate the immune system in different ways and stop tumor cells from growing. Combining different types of biological therapies may kill more tumor cells. PURPOSE: This randomized phase II trial is studying giving vaccine therapy together with dendritic cells to see how well it works compared to giving vaccine therapy together with GM-CSF in treating patients with liver or lung metastases from colorectal cancer removed by surgery.

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miRNA expression microarrays in GM-CSF or GM-CSF+IL6-induced mouse MDSC

Project description:Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. Multiple factors including cytokines, transcription factors and multiple signaling pathways are involved in MDSC differentiation. Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin(IL-6) etc could in vitro mediate development of MDSCs.IL-6 with GM-CSF mediated MDSC not only had stronger suppressive function but also the dynamics of their suppressive function was different from GM-CSF alone mediated MDSCs.To found a new regulatory factor (s) in tumor and inflammatory environments, we compared GM-CSF and IL-6 mediated MDSCs with GM-CSF alone mediated MDSCs using lncRNA microarray, miRNA microarrays and protein-coding mRNA microarrays.

2017-10-09 | GSE104719 | GEO

mRNA and long noncoding RNA expression microarrays in GM-CSF or GM-CSF+IL6-induced mouse MDSC

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NK cell-derived GM-CSF is critical for enhancing pathological arthritis

Project description:GM-CSF is involved in immune complex (IC)-mediated arthritis. However, little is known about what is the cellular source of GM-CSF and how it is regulated during IC-mediated inflammation. Using novel GM-CSF reporter mice, we show that NK cells produce GM-CSF during an IC-mediated model of inflammatory arthritis. NK cells promoted STIA in a GM-CSF-dependent manner, as deletion of NK cells and selective removal of GM-CSF production by NK cells abrogated disease. Furthermore, we show that myeloid cell activation by GM-CSF is restrained by induction of JAK/STAT checkpoint inhibitor cytokine-inducible SH2-containing protein, CIS. Myeloid cells from CIS-deficient mice had exaggerated responses to GM-CSF, and these mice develop exacerbated STIA. Our data suggest that tissue NK cells may amplify joint inflammation in arthritis via GM-CSF production and thus represent a novel target in IC-mediated pathology. Endogenous CIS provides a key brake on signaling through the GM-CSF receptor and strategies that boost its function may provide an alternative anti-inflammatory approach.

2020-02-19 | PXD012794 | Pride

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

Project description:RATIONALE: Colony-stimulating factors, such as GM-CSF, may increase the number of immune cells found in bone marrow or peripheral blood and may help the immune system recover from the side effects of chemotherapy or kill tumor cells. Drugs used in chemotherapy, such as fluorouracil, leucovorin, and oxaliplatin, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Giving more than one drug (combination chemotherapy) may kill more tumor cells. Giving combination chemotherapy after surgery may kill any remaining tumor cells. Sometimes, after surgery, the tumor may not need additional treatment until it progresses. In this case, observation may be sufficient. PURPOSE: This phase II trial is studying how well GM-CSF and combination chemotherapy work in treating patients who are undergoing surgery for stage II or stage III colon cancer.

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Quantitative Proteome Responses to Oncolytic Reovirus in GM-CSF and M-CSF-Differentiated Bone Marrow-Derived Cells

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2020-01-07 | PXD015203 | Pride

Gene expression profiling of mature dendritic cells from mice s. c. treated with GM-CSF-gene transduced LLC cells (LLC/SeV/GM) or control cells (LLC, LLC/SeV/GFP)

Project description:Irradiated granulocyte macrophage-colony stimulating factor (GM-CSF)-transduced autologous tumor cells induce substantial antitumor immunity through the maturation and migration of dendritic cells (DCs). However, little is known about the key molecules involved in GM-CSF-sensitized DCs (GM-DCs) in tumor draining lymph nodes (TDLNs). We initially confirmed that mice subcutaneously injected with poorly immunogenic syngeneic Lewis lung carcinoma (LLC) cells transduced with Sendai virus encoding GM-CSF (LLC/SeV/GM) significantly rejected the tumor growth. Using microarray expression profiling, we obtained a large number of gene expression data files from GM-DCs and control DCs in TDLNs, and subjected them to network-based cluster analysis and unexpectedly unraveled the expression levels of type I IFNs-related genes specifically expressed in plasmacytoid DCs (pDC) were robustly up-regulated in GM-DCs. In vivo depletion assay showed that pDC-depleted mice treated with subcutaneous LLC/SeV/GM cells abrogated the antitumor effects observed in control mice. Moreover combination use of imiquimod for TLR7 triggering on pDC with irradiated LLC/SeV/GM cells induced a significant therapeutic antitumor effect with marked induction of CD9+ pDC with antitumor phenotype, whereas other control mice groups had only minimal to-modest antitumor responses, implicating that this combined vaccine strategy using imiquimod could be promising for improvement of GM-CSF-induced antitumor immunity. Mouse GM-CSF induced gene expression in mature dendritic cells in tumor draining lymph nodes from C57/BL6N female mouse was measured at 2 days after s.c. tumor challenge with GM-CSF gene-transduced LLC cells (LLC/SeV/GM) or control cells (LLC, LLC/SeV/GFP).

2013-09-30 | E-GEOD-43169 | biostudies-arrayexpress

Gene expression profiling of mature dendritic cells from mice s. c. treated with GM-CSF-gene transduced LLC cells (LLC/SeV/GM) or control cells (LLC, LLC/SeV/GFP)

2013-09-30 | GSE43169 | GEO

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Project description:Reactive oxygen species, including RNS, contribute to the control of multiple immune cell functions within the tumor microenvironment (TME). Tumor-infiltrating myeloid cells (TIMs) represent the archetype of tolerogenic cells that actively contribute to dismantle effective immunity against cancer are among the cells most influenced by these molecules. TIMs inhibit T cell functions and promote tumor progression by several mechanisms including the amplification of the oxidative/nitrosative stress within the TME. In tumors, TIM expansion and differentiation is regulated by the granulocyte-macrophage colony-stimulating factor (GM-CSF), which is produced by cancer and immune cells. Nevertheless, the role of GM-CSF in tumors has not yet been fully elucidated. In this study, we show that GM-CSF activity is significantly affected by RNS-triggered post-translational modifications. The nitration of a single tryptophan residue in the sequence of GM-CSF nourishes the expansion of highly immunosuppressive myeloid subsets in tumor-bearing hosts. Importantly, tumors from colorectal cancer patients express higher levels of nitrated tryptophan compared to non-neoplastic tissues. Collectively, our data identify a novel and selective target that can be exploited to remodel the TME and foster protective immunity against cancer.

2021-10-04 | PXD027049 | Pride

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Project description:To elucidate the underlying immune responses elicited by IFNβ and GM-CSF-secreting CT2A cells to brain tumor microenvironment post resection compared to placebo group and non-IFNβ and GM-CSF-secreting CT2A cell group

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