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Enhanced susceptibility of cancer cells to oncolytic rhabdo-virotherapy by expression of Nodamura virus protein B2 as a suppressor of RNA interference

ABSTRACT: Enhanced susceptibility of cancer cells to oncolytic rhabdo-virotherapy by expression of Nodamura virus protein B2 as a suppressor of RNA interference

PROVIDER: PRJNA473911 | ENA |

REPOSITORIES: ENA

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Enhanced susceptibility of cancer cells to oncolytic rhabdo-virotherapy by expression of Nodamura virus protein B2 as a suppressor of RNA interference

Project description:We have evaluated the response of M14 cells to VSV virus expressing eGFP or insect virus B2 protein. We find interferon related genes to be at higher levels when cells are infected with VSV-B2

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Lactobacillus acidophilus potentiates oncolytic virotherapy through modulating gut microbiota homeostasis in hepatocellular carcinoma

Project description:Oncolytic viruses (OVs) hold promise for cancer treatment. However, the antitumor efficacy is limited. Microbiota plays a pivotal role in cancer treatment and its impact on oncolytic virotherapy is unknown. Here, we show that VSVΔ51 has higher antitumor efficacy for hepatocellular carcinoma in the absence of microbiota in female mouse models. VSVΔ51 infection causes microbiota dysbiosis, increasing most of the gut bacteria abundance, while decreasing the commensal Lactobacillus. VSVΔ51 reduced intestinal expression of SLC20A1 that binds to Lactobacillus acidophilus (L. acidophilus) CdpA cell wall protein through IL6-JAK-STAT3 signaling, thereby attenuating attachment and colonization of L. acidophilus. L. acidophilus supplementation confers sensitivity to VSVΔ51 through restoring gut barrier integrity and microbiota homeostasis destroyed by VSVΔ51. In this work, we show that targeting microbiota homostasis holds substantial potential in improving therapeutic outcomes of oncolytic virotherapy

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Enhanced susceptibility of cancer cells to oncolytic rhabdo-virotherapy by expression of Nodamura virus protein B2 as a suppressor of RNA interference.

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Combination with oxaliplatin improves abscopal effect of oncolytic virotherapy through reorganization of intratumoral macrophages

Project description:Oncolytic virotherapy is a unique and promising immunotherapy. In our prior study, a recombinant oncolytic vaccinia virus carrying IL-7 and IL-12 (hIL-7/mIL-12-VV) showed robust antitumor efficacy in both immunogenic CT26.WT and poorly immunogenic Lewis lung carcinoma (LLC) within the treated tumors. However, the efficacy was limited in virus non-treated (distant) LLC tumors. Here we identified oxaliplatin as a powerful combination partner for an oncolytic vaccinia virus to achieve strong efficacy in the virus-injected tumors and the distant tumors. To understand the molecular mechanism of enhanced antitumor efficacy, we evaluated RNA-sequencing signatures in LLC tumors treated with oxaliplatin alone, hIL-7/mIL-12-VV alone and their combination.

2026-07-01 | GSE299506 | GEO

Combination with oxaliplatin improves abscopal effect of oncolytic virotherapy through reorganization of intratumoral macrophages III

Project description:Oncolytic virotherapy is a unique and promising immunotherapy. In our prior study, a recombinant oncolytic vaccinia virus carrying IL-7 and IL-12 (hIL-7/mIL-12-VV) showed robust antitumor efficacy in both immunogenic CT26.WT and poorly immunogenic Lewis lung carcinoma (LLC) within the treated tumors. However, the efficacy was limited in virus non-treated (distant) LLC tumors. Here we identified oxaliplatin as a powerful combination partner for an oncolytic vaccinia virus to achieve strong efficacy in the virus-injected tumors and the distant tumors. To understand the molecular mechanism of abscopal effect of hIL-7/mIL-12-VV in combination with oxaliplatin, we evaluated RNA-sequencing signatures in LLC tumors inoculated in immuno-comprobised mice.

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Combination with oxaliplatin improves abscopal effect of oncolytic virotherapy through reorganization of intratumoral macrophages II

Project description:Oncolytic virotherapy is a unique and promising immunotherapy. In our prior study, a recombinant oncolytic vaccinia virus carrying IL-7 and IL-12 (hIL-7/mIL-12-VV) showed robust antitumor efficacy in both immunogenic CT26.WT and poorly immunogenic Lewis lung carcinoma (LLC) within the treated tumors. However, the efficacy was limited in virus non-treated (distant) LLC tumors. Here we identified oxaliplatin as a powerful combination partner for an oncolytic vaccinia virus to achieve strong efficacy in the virus-injected tumors and the distant tumors. To understand the molecular mechanism of abscopal effect of hIL-7/mIL-12-VV in combination with oxaliplatin, we evaluated RNA-sequencing signatures of LLC tumors on the virus non-treated side.

2026-07-01 | GSE299507 | GEO

Combination with oxaliplatin improves abscopal effect of oncolytic virotherapy through reorganization of intratumoral macrophages [scRNA-seq]

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T cell phenotype changes associated with oncolytic virotherapy combined with Nivolumab

Project description:There is a critical unmet need for safe and efficacious neoadjuvant treatment for cisplatin-ineligible patients with muscle invasive bladder cancer. We launched a Phase 1b study using the combination of intravesical cretostimogene grenadenorepvec (oncolytic serotype 5 adenovirus encoding granulocyte-macrophage colony stimulating factor) with systemic nivolumab in cisplatin-ineligible patients with cT2-4aN0-1M0 muscle invasive bladder cancer. The primary objective was to measure safety and the secondary objective to assess the antitumor efficacy of the combination. No dose limiting toxicity was encountered in 21 patients enrolled and treated. Combination treatment achieved a pathologic complete response rate of 42.1%, which was associated with baseline free E2F activity and tumor mutational burden, but not PD-L1 status. Although T cell infiltration was broadly induced following intravesical oncolytic virotherapy, the formation, enlargement and maturation of tertiary lymphoid structures (TLS) was specifically associated with complete response, supporting the importance of coordinated humoral and cellular immune responses. Together, these results highlight the potential of this combination regimen to enhance therapeutic efficacy in cisplatin-ineligible patients with muscle invasive bladder cancer, warranting its additional study as a neoadjuvant therapeutic option.

2025-09-04 | GSE276366 | GEO

Subclone of resistant CT26 murine tumor shows high sensitivity to VA7 virotherapy: A novel system to study innate immunity and antigen dominance in oncolytic immuno-virotherapy

Project description:Recently, attenuated Semliki Forest virus vector VA7 completely eliminated type I interferon (IFN) unresponsive human U87 glioma xenografts while IFN responsive mouse GL261 and CT-2A gliomas proved refractory to the oncolytic virotherapy. Here we describe in two clones of a well established Balb/c mouse tumor cell line, CT26 murine colon carcinoma, diametrically opposed IFN responsiveness and sensitivity to oncolytic virus. Both CT26WT and CT26LacZ clones secreted biologically active type I IFN in vitro upon infection but virus replication was self-limiting only in CT26WT cells. Total transcriptome sequencing (RNA-Seq) and western blotting experiments revealed that in sharp contrast to CT26LacZ cells, CT26WT cells had strong constitutive expression of 56 different genes associated with pattern recognition and type I interferon signaling pathways, spanning two reported anti-RNA virus gene signatures and22 genes that have been reported to have direct anti-Alphaviral activity. Correspondingly, only CT26LacZ tumors were infectable in vivo, resulting in rapid central necrosis of the tumors by 96 hours post infection and complete tumor eradication both in immunocompetent and in SCID mice. CT26LacZ tumor eradication by oncolysis induced 100% protective immunity against homologous CT26LacZ challenge but only 50% protection against heterologous CT26WT challenge, indicating LacZ immune dominance over shared antigens. We believe the two clone CT26 system described herein constitutes a challenging yet realistic model for clonally and immunologically heterogeneous cancer where a strong therapy efficacy bias toward sensitive tumor subpopulations might falsely predict therapeutic success on a broad patient scale highlighting the necessity of successful pre-screening for responsive tumors. RNA-Seq in CT26 tumor cell line

2014-09-05 | E-GEOD-53001 | biostudies-arrayexpress

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