ArticleMolecular pharmaceutics2017
Novel TREM-1 Inhibitors Attenuate Tumor Growth and Prolong Survival in Experimental Pancreatic Cancer.
Article in Molecular pharmaceutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- TREM-1 as a novel immunotherapeutic target to treat pancreatic ductal adenocarcinoma.Molecular therapy. Oncology · 2025Article
- Understanding the complexity of tumor-associated macrophages: Druggable and therapeutic insights.Acta pharmaceutica Sinica. B · 2025Review
- TREM-1 inhibitor specificity and timing of treatment initiation can impact its therapeutic efficacy in cancer and inflammatory disease.Frontiers in oncology · 2025Article
- Expressional and prognostic value of TREM1 in ovarian cancer: A comprehensive study based on bioinformatics and clinical analysis validation.Journal of Cancer · 2025Article
- Inhibiting triggering receptor expressed on myeloid cells 1 signaling to ameliorate skin fibrosis.JCI insight · 2024Article
- Stored RBC transfusions leads to the systemic inflammatory response syndrome in anemic murine neonates.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The biology of TREM receptors.Nature reviews. Immunology · 2023Review
- Clinically impactful metabolic subtypes of pancreatic ductal adenocarcinoma (PDAC).Frontiers in genetics · 2023Article
- High Expression of Triggering Receptor Expressed on Myeloid Cells 1 Predicts Poor Prognosis in Glioblastoma.OncoTargets and therapy · 2023Article
- Persistent DNA damage and oncogenic stress-induced Trem1 promotes leukemia in mice.Haematologica · 2022Article
- The role of triggering receptor expressed on myeloid cells-1 (TREM-1) in central nervous system diseases.Molecular brain · 2022Review
- Inhibition of TREM-2 Markedly Suppresses Joint Inflammation and Damage in Experimental Arthritis.International journal of molecular sciences · 2022Article
- Triggering Receptors Expressed on Myeloid Cells 1 : Our New Partner in Human Oncology?Frontiers in oncology · 2022Review
- C1QTNF6 promotes oral squamous cell carcinoma by enhancing proliferation and inhibiting apoptosis.Cancer cell international · 2021Article
- Novel ligands and modulators of triggering receptor expressed on myeloid cells receptor family: 2015-2020 updates.Expert opinion on therapeutic patents · 2021Review
- Pancreatic cancer is marked by complement-high blood monocytes and tumor-associated macrophages.Life science alliance · 2021Article
- An Inflammatory Response Related Gene Signature Associated with Survival Outcome and Gemcitabine Response in Patients with Pancreatic Ductal Adenocarcinoma.Frontiers in pharmacology · 2021Article
- Trem1 mediates neuronal apoptosis via interaction with SYK after spinal cord ischemia-reperfusion injury.American journal of translational research · 2021Article
- Bulk and Single-Cell Profiling of Breast Tumors Identifies TREM-1 as a Dominant Immune Suppressive Marker Associated With Poor Outcomes.Frontiers in oncology · 2021Article
- SCHOOL of nature: ligand-independent immunomodulatory peptides.Drug discovery today · 2020Article
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2 authors.
Funding
Abstract
Pancreatic cancer (PC) is a highly lethal cancer with an urgent need to expand the limited treatment options for patients. Tumor-associated macrophages (TAMs) promote tumor aggressiveness and metastasis. High expression of triggering receptor expressed on myeloid cells 1 (TREM-1) on TAMs directly correlates with poor survival in patients with non-small cell lung cancer (NSCLC). We have previously hypothesized that blockade of TREM-1 could be a promising therapeutic strategy to treat cancer and shown that the novel, ligand-independent TREM-1 inhibitory peptides rationally designed using the signaling chain homooligomerization (SCHOOL) strategy suppress NSCLC growth in vivo. Here, we evaluated the therapeutic potential of these inhibitors in three human PC xenograft mouse models. Administration of SCHOOL peptides resulted in a strong antitumor effect achieving an optimal treatment/control (T/C) value of 19% depending on the xenograft and formulation used and persisting even after treatment was halted. The effect correlated significantly with increased survival and suppressed TAM infiltration. The peptides were well-tolerated when deployed either in free form or formulated into lipopeptide complexes for peptide half-life extension and targeted delivery. Finally, blockade of TREM-1 significantly reduced serum levels of interleukin (IL)-1α, IL-6, and macrophage colony-stimulating factor (M-CSF), but not vascular endothelial growth factor, suggesting M-CSF-dependent antitumor mechanisms. Collectively, these promising data suggest that SCHOOL TREM-1-specific peptide inhibitors have a cancer type independent, therapeutically beneficial antitumor activity and can be potentially used as a stand-alone therapy or as a component of combinational therapy for PC, NSCLC, and other solid tumors.
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