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Comprehensive characterization of tumor immune landscape following oncolytic virotherapy by single-cell RNA sequencing

ABSTRACT: Comprehensive characterization of tumor immune landscape following oncolytic virotherapy by single-cell RNA sequencing

PROVIDER: PRJNA774353 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16570235.fastq.gz	Fastqsanger.gz
	SRR16570236.fastq.gz	Fastqsanger.gz
	SRR16570237.fastq.gz	Fastqsanger.gz
	SRR16570238.fastq.gz	Fastqsanger.gz
	SRR16570239.fastq.gz	Fastqsanger.gz

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Comprehensive characterization of tumor immune landscape following oncolytic virotherapy by single-cell RNA sequencing

Project description:single-cell RNA sequencing analysis on carcinomas treated with an HSV-2-based oncolytic virus to characterize the immunogenic changes in the TME

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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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Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

Project description:Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

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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

Single-cell RNA sequencing reveals a strong connection between Gadd45g upregulation and oncolytic HSV infection in tumor tissue

Project description:The oncolytic effect of virotherapy derives from the intrinsic capability of the applied virus in selectively infecting and killing tumor cells. Although oncolytic viruses of various constructions have been shown to efficiently infect and kill tumor cells in vitro, the efficiency of these viruses to exert the same effect on tumor cells within tumor tissues in vivo has not been extensively investigated. Here we report our studies using single-cell RNA sequencing to comprehensively analyze the gene expression profile of tumor tissues following herpes simplex virus 2-based oncolytic virotherapy. Our data revealed the extent and cell types within the tumor microenvironment that could be infected by the virus. Moreover, we observed changes in the expression of cellular genes, including antiviral genes, in response to viral infection. One notable gene found to be upregulated significantly in oncolytic virus-infected tumor cells was Gadd45g, which is desirable for optimal virus replication. These results not only help reveal the precise infection status of the oncolytic virus in vivo, but also provide insight that may lead to the development of new strategies to further enhance the therapeutic efficacy of oncolytic virotherapy.

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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

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Project description:To investigate the ability for pevonedistat to sensitize renal 786-0 carcinoma cells to VSVd51 oncolyic virotherapy, we treated cells with monotherapies or combination and sequencinced the transcriptome for antiviral interferon impact

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T cell phenotype changes associated with oncolytic virotherapy combined with Nivolumab

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Combination of oncolytic Maraba virus with immune checkpoint blockade overcomes therapy resistance in an immunologically cold model of advanced melanoma with dysfunctional T cell receptor signalling

Project description:Oncolytic viruses are promising immunotherapeutic agents, but their efficacy, particularly following intra-tumoural injection, in relation to the size of the targeted tumour, is unclear. Here we show that an oncolytic rhabdovirus, maraba, activates an immune response in human as well as mouse pre-clinical systems, which targets viral as well as tumour-associated antigens. The addition of immune checkpoint blockade to virotherapy is apparent only on the treatment of larger tumours, which have an inherently more immunosuppressive tumour microenvironment, including skewing of T cell receptor engagement with antigen from conventional to regulatory CD4+ cells. Maraba converts the immunologically cold tumour to hot, thus priming the tumour microenvironment for effective αPD1 combination therapy. This study supports the use of maraba oncolytic virotherapy in combination with immune checkpoint inhibitors in melanoma and highlights the impact of the tumour burden on the immune microenvironment and benefit of single agent and combination treatment.

2024-08-08 | GSE270746 | GEO

Itaconate enhances oncolytic virotherapy via multitarget inhibition of antiviral and inflammatory pathways

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