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Poly I:C is a powerful immune adjuvant as a result of its agonist activities on TLR-3, MDA5 and RIG-I. BO-112 is a nanoplexed formulation of Poly I:C complexed with polyethylenimine that causes tumor cell apoptosis showing immunogenic cell death features and which upon intratumoral release results in more prominent tumor infiltration by T lymphocytes. Intratumoral treatment with BO-112 of subcutaneous tumors derived from MC38, 4 T1 and B16-F10 leads to remarkable local disease control dependent on type-1 interferon and gamma-interferon. Some degree of control of non-injected tumor lesions following BO-112 intratumoral treatment was found in mice bearing bilateral B16-OVA melanomas, an activity which was enhanced with co-treatment with systemic anti-CD137 and anti-PD-L1 mAbs. More abundant CD8+ T lymphocytes were found in B16-OVA tumor-draining lymph nodes and in the tumor microenvironment following intratumoral BO-112 treatment, with enhanced numbers of tumor antigen-specific cytotoxic T lymphocytes. Genome-wide transcriptome analyses of injected tumor lesions were consistent with a marked upregulation of the type-I interferon pathway. Inspired by these data, intratumorally delivered BO-112 is being tested in cancer patients (NCT02828098).

Original publication

DOI

10.1186/s40425-019-0568-2

Type

Journal article

Journal

Journal for immunotherapy of cancer

Publication Date

05/2019

Volume

7

Addresses

Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII, 55, 31008, Pamplona, Spain. maznargo@alumni.unav.es.

Keywords

T-Lymphocytes, Cytotoxic, Lymphocytes, Tumor-Infiltrating, Cell Line, Tumor, Animals, Mice, Melanoma, Experimental, Interferon Type I, Poly I-C, Interferon Inducers, Drug Screening Assays, Antitumor, Injections, Intralesional, Gene Expression Profiling, Signal Transduction, Gene Expression Regulation, Neoplastic, Up-Regulation, Female, Tumor Microenvironment