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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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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.

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

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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.

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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

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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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