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Neo-Adjuvant Oncolytic Virotherapy Prior to Surgery Sensitizes Triple-Negative Breast Cancer to Immune Checkpoint Therapy

ABSTRACT: Triple-negative breast cancer (TNBC) is an aggressive disease for which treatment options are limited and associated with severe toxicities. In this experiment we evaluated the response of 2 murine TNBC models to oncolytic Maraba virus infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE104737 | GEO | 2018/10/01

REPOSITORIES: GEO

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Neo-Adjuvant Oncolytic Virotherapy Prior to Surgery Sensitizes Triple-Negative Breast Cancer to Immune Checkpoint Therapy

Project description:Neo-Adjuvant Oncolytic Virotherapy Prior to Surgery Sensitizes Triple-Negative Breast Cancer to Immune Checkpoint Therapy

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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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A Combination of Chemotherapy and Oncolytic Virotherapy Sensitizes Colorectal Adenocarcinoma to Immune Checkpoint Inhibitors in a cDC1-Dependent Manner

Project description:Comparison of transcriptome data in tumors from mice treated with combinations of mitomycin C, oncolytic HSV-1, anti-PD-1 and anti-CTLA-4.

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Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

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Adjuvant oncolytic virotherapy for personalized anti-cancer vaccination.

Project description:By conferring systemic protection and durable benefits, cancer immunotherapies are emerging as long-term solutions for cancer treatment. One such approach that is currently undergoing clinical testing is a therapeutic anti-cancer vaccine that uses two different viruses expressing the same tumor antigen to prime and boost anti-tumor immunity. By providing the additional advantage of directly killing cancer cells, oncolytic viruses (OVs) constitute ideal platforms for such treatment strategy. However, given that the targeted tumor antigen is encoded into the viral genomes, its production requires robust infection and therefore, the vaccination efficiency partially depends on the unpredictable and highly variable intrinsic sensitivity of each tumor to OV infection. In this study, we demonstrate that anti-cancer vaccination using OVs (Adenovirus (Ad), Maraba virus (MRB), Vesicular stomatitis virus (VSV) and Vaccinia virus (VV)) co-administered with antigenic peptides is as efficient as antigen-engineered OVs and does not depend on viral replication. Our strategy is particularly attractive for personalized anti-cancer vaccines targeting patient-specific mutations. We suggest that the use of OVs as adjuvant platforms for therapeutic anti-cancer vaccination warrants testing for cancer treatment.

| S-EPMC8113265 | biostudies-literature

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

Project description:4 octyl itaconate (4-OI) is a known anti-inflammatory chemical that activates Nrf2 signaling. Here, we are exploring the capacities of 4-OI to promote the spread of oncolytic Vesicular Stomatitis Virus (VSVd51M) in pLenti control kidney adenocarcinoma 786-O cell line and in Nrf2 knock out 786-O.

2023-06-15 | GSE232509 | 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

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Enhancing oncolytic virotherapy by extracellular vesicle mediated microRNA reprograming of the tumour microenvironment.

Project description:miRNA expression is critical in driving macrophage polarisation by simultaneously regulating expression of multiple cellular targets. Reintroducing miRNA to promote an anti-tumour macrophage phenotype is a promising therapeutic approach to reverse the immunosuppressive function of tumour associated macrophages.Small RNA sequencing was used to identify differentially expressed miRNA during TAM generation and following LPS/IFNγ stimulation to induce an anti-tumour phenotype. Two differentially expressed miRNA identified, miR-155 and miR-19a, were cloned into oncolytic rhabdovirus (ORV), and anti-tumour efficacy was investigated using both in vitro and in vivo models of OvCa.

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Oncolytic virotherapy induced CSDE1 neo-antigenesis restricts VSV replication but can be targeted by immunotherapy.

Project description:In our clinical trials of oncolytic vesicular stomatitis virus expressing interferon beta (VSV-IFNβ), several patients achieved initial responses followed by aggressive relapse. We show here that VSV-IFNβ-escape tumors predictably express a point-mutated CSDE1P5S form of the RNA-binding Cold Shock Domain-containing E1 protein, which promotes escape as an inhibitor of VSV replication by disrupting viral transcription. Given time, VSV-IFNβ evolves a compensatory mutation in the P/M Inter-Genic Region which rescues replication in CSDE1P5S cells. These data show that CSDE1 is a major cellular co-factor for VSV replication. However, CSDE1P5S also generates a neo-epitope recognized by non-tolerized T cells. We exploit this predictable neo-antigenesis to drive, and trap, tumors into an escape phenotype, which can be ambushed by vaccination against CSDE1P5S, preventing tumor escape. Combining frontline therapy with escape-targeting immunotherapy will be applicable across multiple therapies which drive tumor mutation/evolution and simultaneously generate novel, targetable immunopeptidomes associated with acquired treatment resistance.

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