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- W4313372022 abstract "Abstract Monoclonal antibody (mAb) therapies have greatly improved outcomes for many cancer subtypes, many of which target tumor-associated antigens (TAA). Trastuzumab targets the TAA human epidermal growth factor 2 (HER2), inducing antibody dependent cellular cytotoxicity and phagocytosis (ADCC/ADCP) as well as interfering with receptor signaling. Despite its reputation as the gold standard treatment for HER2-overexpressing cancers, response rates remain low in metastatic breast cancer (≤30% as a monotherapy, ≤50% with chemotherapy). Multiple studies suggest induction of endogenous anti-tumor immunity is a determinant of therapeutic success. Utilizing the genetically heterogeneous Diversity Outbred (DO) mouse model, we seek to identify host-intrinsic mechanisms of resistance to TAA-mediated immunotherapy. We find a divergent response to αNeu (HER2 homolog) mAb clone 7.16.4 in (DOxBALB/c)F1 mice bearing established BALB/c-syngeneic TUBO mammary carcinoma. We find host genetic background regulates anti-tumor immune activity. ~25% showed complete response (CR) to therapy, ~60% a partial response (PR), and ~15% failed to respond (NR). CR mice were protected from a contralateral rechallenge, suggesting adaptive anti-tumor immunity was promoted by mAb therapy. Peripheral anti-tumor IgG, measured by flow cytometry, and IFNγ producing T cells, measured via ELISpot, also trend toward CR>PR>NR. Genetic linkage analysis using R/qtl2 identified loci associated with robust response to mAb therapy. Genes within these loci may represent potential routes of ingress toward addressing innate and acquired resistance during anti-TAA mAb therapy, particularly as regulators of immunogenicity of ADCC and ADCP. NIH R37 CA220482." @default.
- W4313372022 created "2023-01-06" @default.
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- W4313372022 date "2020-05-01" @default.
- W4313372022 modified "2023-09-30" @default.
- W4313372022 title "Identifying host-intrinsic resistance mechanisms to therapeutic anti-tumor antibody" @default.
- W4313372022 doi "https://doi.org/10.4049/jimmunol.204.supp.242.25" @default.
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