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Nanostructured Lipid Carriers based mRNA vaccine leads to a T cell–inflamed tumor microenvironment favorable for improving PD-1/PD-L1 blocking therapy and long-term immunity in a cold tumor model

ABSTRACT: Nanostructured Lipid Carriers based mRNA vaccine leads to a T cell–inflamed tumor microenvironment favorable for improving PD-1/PD-L1 blocking therapy and long-term immunity in a cold tumor model

PROVIDER: PRJNA1188504 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31411713_1.fastq.gz	Fastqsanger.gz
	SRR31411713_2.fastq.gz	Fastqsanger.gz
	SRR31411714_1.fastq.gz	Fastqsanger.gz
	SRR31411714_2.fastq.gz	Fastqsanger.gz
	SRR31411715_1.fastq.gz	Fastqsanger.gz

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Nanostructured Lipid Carriers based mRNA vaccine leads to a T cell–inflamed tumor microenvironment favorable for improving PD-1/PD-L1 blocking therapy and long-term immunity in a cold tumor model

Project description:Using RNA-seq analysis, we have described the impact of a mRNA based vaccine on intratumoral immune-related transcriptional signature in a B16-OVA cold model

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Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans.

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans.

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Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (Visium).

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (Visium).

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Evading immune evasion via reprograming of the tumor microenvironment by radiotherapy and simultaneous targeting of TGF-β/PD-L1

Project description:Tumor immunogenicity enhanced by radiotherapy (RT), is often counterbalanced by immune evasive mechanisms and tissue remodeling effects via upregulation of transforming growth factor-β (TGF-β) and programmed cell death-ligand 1 (PD-L1). We report that bintrafusp alfa (BA), a bifunctional fusion protein that simultaneously inhibits TGF-β and PD-L1, is a favorable combination partner for RT in eradicating multiple treatment-resistant tumor models. Beneficial effects of BA+RT (BART) are partly attributed to counterbalancing undesired RT effects and local tumor microenvironment reprograming, leading to reconstitution of tumor immunity and regression of spontaneous lung metastases. Intriguingly, BA, but neither TGF-β trap nor anti–PD-L1 alone, attenuates late-stage RT-induced lung fibrosis. Single cell transcriptome show TGF-β expression is confined to PD-L1+ endothelium and M2/lipofibroblast-like cells. Hence, superior effects of BA could be attributed to its ability to trap TGF-β to relevant PD-L1+ compartments. Here, we provide rationales that BART resensitizes tumors and broadens the therapeutic window.

2021-08-16 | GSE182004 | GEO

Improving Immunotherapy Responses by Dual Inhibition of Macrophage Migration Inhibitory Factor and PD-1

Project description:Macrophage migration inhibitory factor (MIF) is an upstream regulatory cytokine that is associated with advanced disease and poor outcomes in multiple cancer types, including melanoma. We investigated whether anti-MIF therapy could enhance the antitumor effects of the immune checkpoint inhibitor anti-PD-1 in two murine tumor models. The therapeutic efficacy of anti-MIF, alone or combined with anti-PD-1, was tested in the YUMMER1.7 melanoma and MC38 colorectal cancer models. Tumor growth and survival were assessed in untreated Mif knockout (KO) and low-expression human MIF allele (CATT5) mice and compared to wild-type (WT) or high-expression MIF allele (CATT7) mice. Tumor-bearing animals underwent cytokine profiling, tumor immunohistochemistry, flow cytometry, and single-cell RNA sequencing (scRNA-seq). We also correlated functional variant MIF alleles with melanoma incidence and progression in patients. Our results showed that combined anti-MIF and anti-PD-1 significantly reduced tumor growth, improved survival, and promoted tumor regression, accompanied by enhanced TH1 cytokine levels, macrophage activation, and increased type 1 conventional dendritic cells (cDCs). scRNA-seq analysis revealed an expansion of intra-tumor Cd74/C1q/Aif1-expressing macrophages, which exhibited an antitumor phenotype, in response to anti-MIF therapy. MIF-KO and CATT5 mice exhibited reduced tumor burdens compared to WT or CATT7 mice alone and in the presence of anti-PD-1. In melanoma patients, the high MIF expression genotype (-173C/C) occurred at higher frequencies compared to healthy controls. These findings highlight that the addition of anti-MIF to anti-PD-1 reduces tumor growth, enhances anti-tumor responses, prolongs survival, and augments key intratumor immune cell populations involved in immune activation against tumors. This approach merits further consideration for clinical trial development.

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Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq II).

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq II).

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Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq I).

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq I).

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Expression data in human renal cell carcinoma samples from patients who did or did not respond to anti-PD-1 (Nivolumab) immunotherapy

Project description:Pre-treatment tumor expression of PD-L1 has been shown to correlate with favorable clinical outcomes following PD-1 blocking therapies. However, the majority of patients with PD-L1+ tumors do not respond to treatment. With the goal of obtaining insights into the mechanisms underlying the response to anti-PD-1 targeted therapies in patients with renal cell carcinoma (RCC) with positive tumor expression of PD-L1, microarray expression data was obtained for pre-treatment tumors from patients with RCC who did or did not have a positive response to anti-PD-1 (nivolumab) therapy. Insight into these mechanisms may lead to improved rationally designed therapies, and biomarkers for selecting patients who are more likely to benefit from these treatments. Gene expression profiling was performed on total RNA extracted from 11 formalin-fixed paraffin-embedded (FFPE) RCC specimens, 4 of which were from patients who had a positive response (objective tumor regression) to the anti-PD-1 (nivolumab) immunotherapy, and 7 of which were from patients who did not have a response. Details of the design, and the gene signatures found are given in the paper associated with this GEO Series: Maria Libera Ascierto, Tracee L. McMiller, Alan E. Berger, Ludmila Danilova, Robert A. Anders, George J. Netto, Haiying Xu, Theresa S. Pritchard, Jinshui Fan, Chris Cheadle, Leslie Cope, Charles G. Drake, Drew M. Pardoll, Janis M. Taube, and Suzanne L. Topalian, The Intratumoral Balance between Metabolic and Immunologic Gene Expression Is Associated with Antiâ??PD-1 Response in Patients with Renal Cell Carcinoma, published online in Cancer Immunology Research on 4 August 2016, doi: 10.1158/2326-6066.CIR-16-0072 http://cancerimmunolres.aacrjournals.org/content/early/2016/07/28/2326-6066.CIR-16-0072.full.pdf+html

2016-08-04 | E-GEOD-67501 | biostudies-arrayexpress

Oleuropein reprograms the immunosuppressive footprint of tumor-associated myeloid cells and enhances PD-L1/PD-1 blockade immunotherapy in cancer

Project description:Therapies based on PD-1/PD-L1 blockade fail in most cancer patients. Here we evaluated the capacities of oleuropein to reprogram tumor-associated immunosuppressive myeloid cells to increase the potency of immunotherapies. Oleuropein caused major global reprogramming of monocytic and granulocytic myeloid-derived suppressor cells and tumor-associated macrophages towards immunostimulatory subsets. Differential quantitative proteomics uncovered activated and down-modulated pathways at high resolution for each subset which regulated major differentiation programs. Oleuropein significantly potentiated the capacities of myeloid cells to activate T-cells and enhanced antitumor properties of PD-1 blockade, either by systemic anti-PD-1 antibody administration, or locally by intratumor antibody delivery with a self-amplifying RNA vector based on Semliki Forest virus. Combination therapies decreased tumor infiltration by immunosuppressive myeloid cells and increased dendritic cell recruitment within draining lymph nodes, leading to systemic antitumor T-cell responses. Potent therapeutic activities were evident in lung cancer models resistant to immunotherapies and in colon cancer models.

2024-12-08 | PXD047616 | JPOST Repository

Expression data in PD-L1 positive and PD-L1 negative human melanoma samples

Project description:Blocking the PD-1/PD-L1 immunosuppressive pathway has shown promise in the treatment of certain cancers including melanoma. This study investigates differences in the gene expression profiles of human melanomas that do or do not display the immunosuppressive protein PD-L1. Further understanding of genes expressed within the tumor microenvironment of PD-L1+ tumors may lead to improved rationally designed treatments. Gene expression profiling was performed on total RNA extracted by laser capture microdissection from 11 archived formalin-fixed paraffin-embedded (FFPE) melanoma specimens, 5 of which were PD-L1 positive and 6 PD-L1 negative. Details of the design, and the gene signatures found are given in the paper associated with this GEO Series: Janis M. Taube, Geoffrey D. Young, Tracee L. McMiller, Shuming Chen, January T. Salas, Theresa S. Pritchard, Haiying Xu, Alan K. Meeker, Jinshui Fan, Chris Cheadle, Alan E. Berger, Drew M. Pardoll, and Suzanne L. Topalian, Differential expression of immune-regulatory genes associated with PD-L1 display in melanoma: implications for PD-1 pathway blockade, Clin Cancer Res 2015, in press.

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