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Topical TLR7 agonist and radiotherapy in patients with metastatic breast cancer

ABSTRACT: Topical TLR7 agonist and radiotherapy in patients with metastatic breast cancer

PROVIDER: PRJNA1188592 | ENA |

REPOSITORIES: ENA

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Topical TLR7 agonist and radiotherapy in patients with metastatic breast cancer

Project description:This study explores the safety and efficacy of combining topical Imiquimod (IMQ), a TLR-7 agonist, with local radiotherapy (RT) for metastatic breast cancer. The phase I/II clinical trial (NCT01421017) aimed to assess systemic and local anti-tumor responses using immune-related response criteria (irRC). Patients were divided into three cohorts: (1) IMQ + RT + cyclophosphamide, (2) IMQ + RT, and (3) RT + cyclophosphamide (control). Cutaneous metastases were treated with IMQ+RT (area A) or IMQ alone (area B). Tumor biopsies were obtained at baseline and after treatment for gene expression profiling. Results demonstrated safety and promising systemic anti-tumor responses, with transcriptional analyses revealing a T-helper 1 immune orientation and DNA-repair gene downregulation associated with complete responses in IMQ+RT-treated areas.

2025-04-16 | GSE282443 | GEO

Topical TLR7 agonist and radiotherapy in patients with metastatic breast cancer.

Project description: Not available

| S-EPMC11973781 | biostudies-literature

TLR7 Agonist Nanomedicine Suppresses Lung Metastasis of Osteosarcoma by Remodeling the Immune Microenvironment

Project description:This study aimed to evaluate a TLR7 agonist liposome (1V209-Cho-Lip) for its anti-metastatic effects and mechanisms in osteosarcoma. Single-cell transcriptomics analysis demonstrated that treatment with 1V209-Cho-Lip alleviates myeloid-mediated immunosuppression, promotes CD8+ T cell activation and clonal expansion, and improves intercellular communication between tumor cells and immune cells.

2026-08-12 | GSE342815 | GEO

Stimulation of isolated plasmacytoid dendritic cells (pDCs) with TLR9 agonist CpG C (CpG) and TLR7 agonist imiquimod (IMQ)

Project description:The purpose of this experiment was to assess the genes upregulated when pDCs were stimulated with TLR7 agonist imiquimod and TLR9 agonist CpG C.

2016-03-17 | GSE79272 | GEO

Stimulation of isolated plasmacytoid dendritic cells (pDCs) with TLR9 agonist CpG C (CpG) and TLR7 agonist imiquimod (IMQ)

Project description:The purpose of this experiment was to assess the genes upregulated when pDCs were stimulated with TLR7 agonist imiquimod and TLR9 agonist CpG C. pDCs were isolated from six healthy donors by FACS sorting, and were stimulated with CpG and imiquimod for 18 hours, after which RNA was extracted for next generation sequencing on the Illumina HiSeq platform. Unstimulated samples were included as controls.

2016-03-17 | E-GEOD-79272 | biostudies-arrayexpress

Synthetic TLR7/8 agonist bottlebrush prodrugs enable tumor-selective immune stimulation following systemic administration

Project description:We used single cell RNA sequencing to understand how the tumor microenvironment changes with TLR7/8 agonist bottlebrush

2023-04-26 | GSE224626 | GEO

Treatment of human monocytes with TLR7 or TLR8 agonists

Project description:Goal was to detect differences in response to TLR7 versus TLR8 agonists in human monocytes from healthy donors 3 deidentified donors from the Red Cross, monocytes from each donor incubated overnight with either vehicle, TLR7 agonist or TLR8 agonist

2014-12-24 | E-GEOD-64480 | biostudies-arrayexpress

TLR7/8 Agonist Treatment Induces an Increase in Bone Marrow Resident Dendritic Cells and Hematopoietic Progenitor Expansion and Mobilization

Project description:Treatment with the TLR7/8 agonist R848 results in a significant increase in classic dendritic cells (DCs) in the bone marrow, but a decrease in common dendritic cell progenitors and pre-DCs. Phenotypic analysis of DCs showed that R848 treatment is associated with altered expression of certain chemokines, activation markers, and migratory receptors.

2021-02-01 | GSE163600 | GEO

UNC93B1 variants underlie TLR7-dependent autoimmunity

Project description:UNC93B1 is critical for trafficking and function of nucleic acid-sensing Toll-like receptors (TLRs) TLR3, TLR7, TLR8, and TLR9, which are essential for antiviral immunity. Overactive TLR7 signaling induced by recognition of self-nucleic acids has been implicated in systemic lupus erythematosus (SLE). Here, we report UNC93B1 variants (E92G and R336L) in four patients with early-onset SLE. Patient cells or mouse macrophages carrying the UNC93B1 variants produced high amounts of TNF-α and IL-6 and upon stimulation with TLR7/TLR8 agonist, but not with TLR3 or TLR9 agonists. E92G causes UNC93B1 protein instability and reduced interaction with TLR7, leading to selective TLR7 hyperactivation with constitutive type I IFN signaling. Thus, UNC93B1 regulates TLR subtype-specific mechanisms of ligand recognition. Our findings establish a pivotal role for UNC93B1 in TLR7-dependent autoimmunity and highlight the therapeutic potential of targeting TLR7 in SLE.

2023-12-14 | GSE250223 | GEO

Bruton's Tyrosine Kinase Regulates TLR9 but not TLR7 Signaling in Human pDCs

Project description:Plasmacytoid dendritic cells (pDCs) can be activated by the endosomal TLRs, and contribute to the pathogenesis of systemic lupus erythematosus (SLE) by producing type I IFNs. Thus, blocking TLR-mediated pDC activation may represent a useful approach for the treatment of SLE. In an attempt to identify a therapeutic target for blocking TLR signaling in pDCs, we investigated the contribution of Bruton's tyrosine kinase (Btk) to the activation of pDCs by TLR7 and TLR9 stimulation by using a selective Btk inhibitor RN486. Stimulation of TLR7 and 9 with their respective agonist, namely, gardiquimod and type A CpG ODN2216, resulted in the activation of human pDCs, as demonstrated by the expression of activation markers (CD69, CD40, and CD86), elevated production of IFN-alpha and other inflammatory cytokines, as well as up-regulation of numerous genes including IFN-alpha-inducible genes and activation of interferon regulatory factor 7 (IRF7) and NF-kB. RN486 inhibited all of these events induced by TLR9, but not TLR7 stimulation, with a nanomolar potency for inhibiting type A CpG ODN2216-mediated production of cytokines (e.g., IC50=386 nM for inhibiting IFN-alpha). Our data reveal Btk as an important regulatory enzyme in the TLR9 pathway, and a potential therapeutic target for SLE and other TLR-driven diseases. pDCs from healthy donors (n=4) were treated with gardiquimod (TLR7 agonist) or ODN 2216 (TLR9 agonist) with or without BTK inhibitor for 3 hours.

2015-10-24 | E-GEOD-41825 | biostudies-arrayexpress

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