ArticleScientific reports2026
Application of group A streptococcal collagen-like protein 1-expressing Lactococcus as a novel immunotherapeutic against pancreatic ductal adenocarcinoma.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a fatal malignancy characterized by an immunosuppressive tumor environment. Neutrophil extracellular traps (NETs) have gained recognition in playing a critical role in cancer progression and formulation of the PDAC TME, making them a target for novel PDAC therapies. Herein, we utilize a Lactococcus strain expressing group A streptococcal collagen-like protein 1 (Scl1) to stimulate anti-tumor immunity and inhibit cancer promoting NETs. Orthotopically implanted male and female C57BL6/J or NET-deficient PAD4−/− mice were intra-tumorally or intra-peritoneally injected with Lactococcus wild-type lacking Scl1, Scl1-producing Lactococcus::620, or PBS control. Sera were collected to assess circulating NET markers. A decreased tumor burden, as well as infiltration of anti-tumor CD8 + T and dendritic cells was observed in mice treated with Scl1-expressing Lactococcus::620 compared to Lactococcus wild-type and PBS control. Mice treated with Lactococcus::620 showed reduced cell-free DNA in their sera as a marker for decreased NETosis. These effects were abrogated in PAD4−/− mice, suggesting a NET-dependent anti-tumor effect by Scl1. This study demonstrates a novel therapeutic concept against PDAC using an engineered Scl1-expressing Lactococcus strain. Our results advocate for Scl1-based cancer therapy as an immunomodulator of the PDAC tumor microenvironment.
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