Homo sapiens
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PROVIDER: PRJNA139213 | ENA |
REPOSITORIES: ENA
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Project description:Oncolytic viral therapy represents an alternative therapeutic strategy for the treatment of cancer. This therapy relies on efficient replication of virus in tumor cells in vivo with minimal or no replication in normal tissues. We recently described GLV-1h68 as a modified Vaccinia Virus (VACV) construct with exclusive in vivo tropism for tumor cells in experimental animal models. Moreover, we had previously observed a cell line-specific relationship between the ability of GLV-1h68 to replicate in vitro during the first 20 hours following infection and the in vivo ability to colonize and eliminate the corresponding tumor implant. Thus, we surveyed the in vitro permissivity to GLV-1h68 replication of the NCI-60 panel of cell lines, extensively characterized and used for the assessment of novel therapeutic modalities. All cell lines were cultured and infected in identical conditions. Pre-infection transcriptional profiling was obtained to search for correlates of permissivity to viral infection. Selected cell lines were also tested for permissivity to another VACV and a vesicular stomatitis virus (VSV) strain. We observed that permissivity to VACV infection during the first 20 hours is quite heterogeneous among cell lines but highly reproducible within each cell line. The tissue of origin of each cell line does not influence permissivity to infection with the exception of B cell derivation. Permissivity correlates between two VACV constructs and between them and VSV suggesting a common permissive phenotype. No clear transcriptional pattern predictive of permissivity to infection could be identified though weak associations were observed that suggest a multifactorial control of viral replication. This study adds to the current characterization of the NCI-60 panel to guide the design and interpretation of experimental models testing oncolytic therapies. Seventy-four microarray samples were obtained from 8 renal cancer cell lines (786-0, A498, ACHN, CAKI-I, RXF-393, SN12C, TK-10, UO-31); 12 melanoma cell lines (888-MEL, 1858-MEL, 1936-MEL, 397, A375-MEL, LOX IMVI, M14, SK-MEL-2, SK-MEL-5, SK-MEL-28, UACC 62, UACC 257 ); 11 lung cancer cell lines (A549 p7, A549 p107, EKVX, HOP-62, HOP-92, NCI-H23, NCI-H226, NCI-H322M, NCI-H460, NCI-H522, NCI-H1299); 13 colon cancer cell lines (HCT-15, HCT-116, HT-29 p155, HT-29 p9, KM-12, SW-620, Colo 205, HCC 2998, NCI-ADR-RES, OVCAR 3 p7, OVCAR 3 p42, OVCAR 5, SK-OV-3); 3 ovarian cancer cell lines (OVCAR 4, OVCAR 8, IGROV); 1 cervical cancer cell line (Siha); 6 brain cancer cell lines (SNB 19, SF 295, SF 298, SNB 75, U251, SF 539); 7 breast cancer cell lines (BT-549, GI101A, HS-578T, MCF 7, MDA-MB-231 p41, MDA-MB-435, MDA-MB-231 p6); 7 hematopoietic cancer cell lines (CCFR-CEM, HL-60, K-562, MOLT-4, RPMI 8226, SR, T-47D); 3 prostatic cancer cell lines (Du-145, PC 3 p7, PC 3 p35); 1 hepatic cancer cell lines (Huh 7.5.1); and 2 pancreatic cancer cell lines (MIA PACA 2, Panc 1). Two technical repeats were performed (cell lines Siha and SNB-19). Reference T-RNA was obtained from 6 normal donor PBMCs.
2012-03-24 | E-GEOD-28472 | biostudies-arrayexpress
Project description:Human melanoma tumor cells (HS294T) and monocytes (THP-1) were infected with a double deleted (-VGF, -TK) oncolytic vaccinia virus expressing human DAI (DNA-dependent activator of interferon-regulatory factors). Total RNA was collected and gene expresson profiles were determined with Agilent microarray. An oncolytic vaccinia virus that does not express DAI was used to control the effect of DAI and uninfected cells (PBS treated) were used to control the effect of virus infection. In oncolytic virotherapy the ability of the virus to activate the immune system against tumors is nowadays generally understood to be a key mechanism in full eradication of cancer and for long-term anti-tumor effects. We armed an oncolytic vaccinia virus with DAI to increase the immunogenicity and the vaccine potency of the virus. The aim of this study was to study if the expression of DAI by a replicating vaccinia virus would alter the gene expression profile of infected cells and to study what are the differentially expressed genes. Three-condition experiment: vvdd-tdTomato-hDAI vs. vvdd-tdTomato vs. PBS treated cells. 2 cell lines: HS294T tumor cells and THP-1 monocytes. 3 biological replicates of virus infected cells per cell line and 2 uninfected replicates per cell line. HS294T and THP-1 cells were treated with vvdd-tdTomato-hDAI or vvdd-tdTomato control virus, or with PBS only to have an uninfected control. 16 hours after infection total RNA was extracted and whole genome gene pfofiles were analyzed and differentially expressed genes determined.
2016-03-01 | E-GEOD-76208 | biostudies-arrayexpress
Project description:Oncolytic viral therapy represents an alternative therapeutic strategy for the treatment of cancer. This therapy relies on efficient replication of virus in tumor cells in vivo with minimal or no replication in normal tissues. We recently described GLV-1h68 as a modified Vaccinia Virus (VACV) construct with exclusive in vivo tropism for tumor cells in experimental animal models. Moreover, we had previously observed a cell line-specific relationship between the ability of GLV-1h68 to replicate in vitro during the first 20 hours following infection and the in vivo ability to colonize and eliminate the corresponding tumor implant. Thus, we surveyed the in vitro permissivity to GLV-1h68 replication of the NCI-60 panel of cell lines, extensively characterized and used for the assessment of novel therapeutic modalities. All cell lines were cultured and infected in identical conditions. Pre-infection transcriptional profiling was obtained to search for correlates of permissivity to viral infection. Selected cell lines were also tested for permissivity to another VACV and a vesicular stomatitis virus (VSV) strain. We observed that permissivity to VACV infection during the first 20 hours is quite heterogeneous among cell lines but highly reproducible within each cell line. The tissue of origin of each cell line does not influence permissivity to infection with the exception of B cell derivation. Permissivity correlates between two VACV constructs and between them and VSV suggesting a common permissive phenotype. No clear transcriptional pattern predictive of permissivity to infection could be identified though weak associations were observed that suggest a multifactorial control of viral replication. This study adds to the current characterization of the NCI-60 panel to guide the design and interpretation of experimental models testing oncolytic therapies.
2012-03-24 | GSE28472 | GEO
Project description:Agilent-013282 array CGH on NCI-60 cancer cell lines
| PRJNA210692 | ENA
Project description:Illumina Human1Mv1_C array CGH on NCI-60 cancer cell lines
| PRJNA206552 | ENA
Project description:Nimblegen 385K array CGH on NCI-60 cancer cell lines
| PRJNA143597 | ENA
Project description:Human melanoma tumor cells (HS294T) and monocytes (THP-1) were infected with a double deleted (-VGF, -TK) oncolytic vaccinia virus expressing human DAI (DNA-dependent activator of interferon-regulatory factors). Total RNA was collected and gene expresson profiles were determined with Agilent microarray. An oncolytic vaccinia virus that does not express DAI was used to control the effect of DAI and uninfected cells (PBS treated) were used to control the effect of virus infection. In oncolytic virotherapy the ability of the virus to activate the immune system against tumors is nowadays generally understood to be a key mechanism in full eradication of cancer and for long-term anti-tumor effects. We armed an oncolytic vaccinia virus with DAI to increase the immunogenicity and the vaccine potency of the virus. The aim of this study was to study if the expression of DAI by a replicating vaccinia virus would alter the gene expression profile of infected cells and to study what are the differentially expressed genes.
2016-03-01 | GSE76208 | GEO
Project description:We investigated the mechanisms by which inflammatory responses generated by tumor-specific T cells delivered to ovarian tumor-bearing mice alone or after oncolytic vaccinia virus-driven immunogenic cancer cell death affect antitumor efficacy using spatial transcriptomics.
2024-10-15 | GSE274509 | GEO