RNA-seq of 11 human glioblastoma cell lines under standard serum-containing conditions
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE317583 | GEO | 2026/01/31
REPOSITORIES: GEO
Similar Datasets
Project description:To investigate whether IDH1 mutation influence the effects of oncolytic virus VSVΔ51, we transduced doxycycline-inducible IDH1-R132H lentiviruses into LN-229 to establish the LN-229-TRE-R132H cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of LN-229-TRE-R132H cells infected with or without VSVΔ51 in the presence or absence of IDH1 mutation induced by doxycycline.
2023-09-19 | GSE208634 | GEO
Project description:RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells
| PRJNA579353 | ENA
Project description:Introduction: Brincidofovir (BCV) is a novel nucleoside phosphonate analogue with unique dual anti-viral and anti-tumor properties. Results: BCV demonstrated potent anti-tumor activity in vitro across the majority of cell-lines regardless of EBV positivity, with IC50 values within clinically-achievable human plasma concentrations (2 µg/ml) in 17/25 (68.0%) T/NK-NHL and in 13/19 (68.4%) BCL. In vivo treatment via intraperitoneal BCV (IP, 40mg/kg, 2X per week) significantly inhibited tumor growth in all xenograft models when compared to vehicle control. Notably, RNAseq analysis demonstrated BCV downregulated MYC and MYC-target pathways in T/NK-NHL models. Further mechanistic studies showed that BCV evoked S-phase cell cycle arrest, replication stress, DNA damage and apoptosis, while also triggering STING pathway-mediated interferon responses, PD-L1 expression and immunogenic cell death. In the syngeneic EL4-C57BL/6 model, BCV in combination with anti-PD1 significantly inhibited tumor growth and triggered an immune reaction characterized by highest scores for adaptive immune response, cytokines/chemokines & receptors, cytotoxic cells, dendritic cells, NK CD56dim cells and neutrophils (NanoString Immunology Panel). Conclusions: Taken together, these results demonstrate a novel role of BCV in the treatment of lymphoma, and suggest potential for combination with checkpoint immunotherapy.
2026-03-18 | GSE293367 | GEO
Project description:JMJD1C shows ubiquitous expression and is often downregulated in tumor entities compared to healthy tissues.JMJD1C inhibit growth of the glioblastoma cell line LN-229. Here, JMJD1C knockdown leads to malignant progression in the glioblastoma cell line LN-229.
2021-02-09 | GSE166351 | GEO
Project description:Introduction: Brincidofovir (BCV) is a novel nucleoside phosphonate analogue with unique dual anti-viral and anti-tumor properties. Methods: Activity of BCV was evaluated in forty-four cell-line models, including T/NK-NHL (n=25) and B-cell lymphoma (BCL, n=19), as well as their respective NOD/SCID mice xenograft models (NK/T-cell lymphoma, peripheral T-cell lymphoma, not otherwise specified, TP63-rearranged anaplastic large cell lymphoma, and MYC/BCL2-rearranged diffuse large B-cell lymphoma). Potential in vivo immunogenic effects were examined in a syngeneic EL4-C57BL/6 murine lymphoma model. Results: BCV demonstrated potent anti-tumor activity in vitro across the majority of cell-lines regardless of EBV positivity, with IC50 values within clinically-achievable human plasma concentrations (2 µg/ml) in 17/25 (68.0%) T/NK-NHL and in 13/19 (68.4%) BCL. In vivo treatment via intraperitoneal BCV (IP, 40mg/kg, 2X per week) significantly inhibited tumor growth in all xenograft models when compared to vehicle control. Notably, RNAseq analysis demonstrated BCV downregulated MYC and MYC-target pathways in T/NK-NHL models. Further mechanistic studies showed that BCV evoked S-phase cell cycle arrest, replication stress, DNA damage and apoptosis, while also triggering STING pathway-mediated interferon responses, PD-L1 expression and immunogenic cell death. In the syngeneic EL4-C57BL/6 model, BCV in combination with anti-PD1 significantly inhibited tumor growth and triggered an immune reaction characterized by highest scores for adaptive immune response, cytokines/chemokines & receptors, cytotoxic cells, dendritic cells, NK CD56dim cells and neutrophils (NanoString Immunology Panel). Conclusions: Taken together, these results demonstrate a novel role of BCV in the treatment of lymphoma, and suggest potential for combination with checkpoint immunotherapy.
2026-03-18 | GSE295563 | GEO
Project description:Introduction: Brincidofovir (BCV) is a novel nucleoside phosphonate analogue with unique dual anti-viral and anti-tumor properties. Methods: Activity of BCV was evaluated in forty-four cell-line models, including T/NK-NHL (n=25) and B-cell lymphoma (BCL, n=19), as well as their respective NOD/SCID mice xenograft models (NK/T-cell lymphoma, peripheral T-cell lymphoma, not otherwise specified, TP63-rearranged anaplastic large cell lymphoma, and MYC/BCL2-rearranged diffuse large B-cell lymphoma). Potential in vivo immunogenic effects were examined in a syngeneic EL4-C57BL/6 murine lymphoma model. Results: BCV demonstrated potent anti-tumor activity in vitro across the majority of cell-lines regardless of EBV positivity, with IC50 values within clinically-achievable human plasma concentrations (2 µg/ml) in 17/25 (68.0%) T/NK-NHL and in 13/19 (68.4%) BCL. In vivo treatment via intraperitoneal BCV (IP, 40mg/kg, 2X per week) significantly inhibited tumor growth in all xenograft models when compared to vehicle control. Notably, RNAseq analysis demonstrated BCV downregulated MYC and MYC-target pathways in T/NK-NHL models. Further mechanistic studies showed that BCV evoked S-phase cell cycle arrest, replication stress, DNA damage and apoptosis, while also triggering STING pathway-mediated interferon responses, PD-L1 expression and immunogenic cell death. In the syngeneic EL4-C57BL/6 model, BCV in combination with anti-PD1 significantly inhibited tumor growth and triggered an immune reaction characterized by highest scores for adaptive immune response, cytokines/chemokines & receptors, cytotoxic cells, dendritic cells, NK CD56dim cells and neutrophils (NanoString Immunology Panel). Conclusions: Taken together, these results demonstrate a novel role of BCV in the treatment of lymphoma, and suggest potential for combination with checkpoint immunotherapy.
2026-03-18 | GSE295562 | GEO
Project description:Introduction: Brincidofovir (BCV) is a novel nucleoside phosphonate analogue with unique dual anti-viral and anti-tumor properties. Methods: Activity of BCV was evaluated in forty-four cell-line models, including T/NK-NHL (n=25) and B-cell lymphoma (BCL, n=19), as well as their respective NOD/SCID mice xenograft models (NK/T-cell lymphoma, peripheral T-cell lymphoma, not otherwise specified, TP63-rearranged anaplastic large cell lymphoma, and MYC/BCL2-rearranged diffuse large B-cell lymphoma). Potential in vivo immunogenic effects were examined in a syngeneic EL4-C57BL/6 murine lymphoma model. Results: BCV demonstrated potent anti-tumor activity in vitro across the majority of cell-lines regardless of EBV positivity, with IC50 values within clinically-achievable human plasma concentrations (2 µg/ml) in 17/25 (68.0%) T/NK-NHL and in 13/19 (68.4%) BCL. In vivo treatment via intraperitoneal BCV (IP, 40mg/kg, 2X per week) significantly inhibited tumor growth in all xenograft models when compared to vehicle control. Notably, RNAseq analysis demonstrated BCV downregulated MYC and MYC-target pathways in T/NK-NHL models. Further mechanistic studies showed that BCV evoked S-phase cell cycle arrest, replication stress, DNA damage and apoptosis, while also triggering STING pathway-mediated interferon responses, PD-L1 expression and immunogenic cell death. In the syngeneic EL4-C57BL/6 model, BCV in combination with anti-PD1 significantly inhibited tumor growth and triggered an immune reaction characterized by highest scores for adaptive immune response, cytokines/chemokines & receptors, cytotoxic cells, dendritic cells, NK CD56dim cells and neutrophils (NanoString Immunology Panel). Conclusions: Taken together, these results demonstrate a novel role of BCV in the treatment of lymphoma, and suggest potential for combination with checkpoint immunotherapy.
2026-03-18 | GSE295561 | GEO
Project description:Introduction: Brincidofovir (BCV) is a novel nucleoside phosphonate analogue with unique dual anti-viral and anti-tumor properties. Methods: Activity of BCV was evaluated in forty-four cell-line models, including T/NK-NHL (n=25) and B-cell lymphoma (BCL, n=19), as well as their respective NOD/SCID mice xenograft models (NK/T-cell lymphoma, peripheral T-cell lymphoma, not otherwise specified, TP63-rearranged anaplastic large cell lymphoma, and MYC/BCL2-rearranged diffuse large B-cell lymphoma). Potential in vivo immunogenic effects were examined in a syngeneic EL4-C57BL/6 murine lymphoma model. Results: BCV demonstrated potent anti-tumor activity in vitro across the majority of cell-lines regardless of EBV positivity, with IC50 values within clinically-achievable human plasma concentrations (2 µg/ml) in 17/25 (68.0%) T/NK-NHL and in 13/19 (68.4%) BCL. In vivo treatment via intraperitoneal BCV (IP, 40mg/kg, 2X per week) significantly inhibited tumor growth in all xenograft models when compared to vehicle control. Notably, RNAseq analysis demonstrated BCV downregulated MYC and MYC-target pathways in T/NK-NHL models. Further mechanistic studies showed that BCV evoked S-phase cell cycle arrest, replication stress, DNA damage and apoptosis, while also triggering STING pathway-mediated interferon responses, PD-L1 expression and immunogenic cell death. In the syngeneic EL4-C57BL/6 model, BCV in combination with anti-PD1 significantly inhibited tumor growth and triggered an immune reaction characterized by highest scores for adaptive immune response, cytokines/chemokines & receptors, cytotoxic cells, dendritic cells, NK CD56dim cells and neutrophils (NanoString Immunology Panel). Conclusions: Taken together, these results demonstrate a novel role of BCV in the treatment of lymphoma, and suggest potential for combination with checkpoint immunotherapy.
2026-03-18 | GSE295564 | GEO
Project description:Introduction: Brincidofovir (BCV) is a novel nucleoside phosphonate analogue with unique dual anti-viral and anti-tumor properties. Methods: Activity of BCV was evaluated in forty-four cell-line models, including T/NK-NHL (n=25) and B-cell lymphoma (BCL, n=19), as well as their respective NOD/SCID mice xenograft models (NK/T-cell lymphoma, peripheral T-cell lymphoma, not otherwise specified, TP63-rearranged anaplastic large cell lymphoma, and MYC/BCL2-rearranged diffuse large B-cell lymphoma). Potential in vivo immunogenic effects were examined in a syngeneic EL4-C57BL/6 murine lymphoma model. Results: BCV demonstrated potent anti-tumor activity in vitro across the majority of cell-lines regardless of EBV positivity, with IC50 values within clinically-achievable human plasma concentrations (2 µg/ml) in 17/25 (68.0%) T/NK-NHL and in 13/19 (68.4%) BCL. In vivo treatment via intraperitoneal BCV (IP, 40mg/kg, 2X per week) significantly inhibited tumor growth in all xenograft models when compared to vehicle control. Notably, RNAseq analysis demonstrated BCV downregulated MYC and MYC-target pathways in T/NK-NHL models. Further mechanistic studies showed that BCV evoked S-phase cell cycle arrest, replication stress, DNA damage and apoptosis, while also triggering STING pathway-mediated interferon responses, PD-L1 expression and immunogenic cell death. In the syngeneic EL4-C57BL/6 model, BCV in combination with anti-PD1 significantly inhibited tumor growth and triggered an immune reaction characterized by highest scores for adaptive immune response, cytokines/chemokines & receptors, cytotoxic cells, dendritic cells, NK CD56dim cells and neutrophils (NanoString Immunology Panel). Conclusions: Taken together, these results demonstrate a novel role of BCV in the treatment of lymphoma, and suggest potential for combination with checkpoint immunotherapy.
2026-03-18 | GSE295560 | GEO
Project description:Introduction: Brincidofovir (BCV) is a novel nucleoside phosphonate analogue with unique dual anti-viral and anti-tumor properties. Methods: Activity of BCV was evaluated in forty-four cell-line models, including T/NK-NHL (n=25) and B-cell lymphoma (BCL, n=19), as well as their respective NOD/SCID mice xenograft models (NK/T-cell lymphoma, peripheral T-cell lymphoma, not otherwise specified, TP63-rearranged anaplastic large cell lymphoma, and MYC/BCL2-rearranged diffuse large B-cell lymphoma). Potential in vivo immunogenic effects were examined in a syngeneic EL4-C57BL/6 murine lymphoma model. Results: BCV demonstrated potent anti-tumor activity in vitro across the majority of cell-lines regardless of EBV positivity, with IC50 values within clinically-achievable human plasma concentrations (2 µg/ml) in 17/25 (68.0%) T/NK-NHL and in 13/19 (68.4%) BCL. In vivo treatment via intraperitoneal BCV (IP, 40mg/kg, 2X per week) significantly inhibited tumor growth in all xenograft models when compared to vehicle control. Notably, RNAseq analysis demonstrated BCV downregulated MYC and MYC-target pathways in T/NK-NHL models. Further mechanistic studies showed that BCV evoked S-phase cell cycle arrest, replication stress, DNA damage and apoptosis, while also triggering STING pathway-mediated interferon responses, PD-L1 expression and immunogenic cell death. In the syngeneic EL4-C57BL/6 model, BCV in combination with anti-PD1 significantly inhibited tumor growth and triggered an immune reaction characterized by highest scores for adaptive immune response, cytokines/chemokines & receptors, cytotoxic cells, dendritic cells, NK CD56dim cells and neutrophils (NanoString Immunology Panel). Conclusions: Taken together, these results demonstrate a novel role of BCV in the treatment of lymphoma, and suggest potential for combination with checkpoint immunotherapy.
2026-03-18 | GSE295559 | GEO