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863 results for “immune checkpoints”
RNA datasets to derive predictors for immune checkpoint inhibitor therapy of non-small cell lung cancer
<p>Nanostring nCounter datasets and corresponding clinical data of tumor samples of patients with advanced NSCLC who received anti-PD-1 immuntherapy. Prospectively divided into a discovery and a validation cohort.</p> <p>Please cite the corresponding publication in Annals of Oncology (10.1093/annonc/mdz049)</p>
NanoString dataset for study: Impairment of cancer-associated fibroblasts promotes CD8+ T cell infiltration and enhances sensitivity to immune checkpoint blockade
<p>Pre-processed NanoString mRNA abundance data and associated sample sheet for study:</p> <p>Impairment of cancer-associated fibroblasts promotes CD8+ T cell infiltration and enhances sensitivity to immune checkpoint blockade</p>
Conserved angio-immune subtypes of the cancer microenvironment predict response to immune checkpoint blockade therapy
<p>Immune checkpoint blockade (ICB) therapy has revolutionized cancer treatment. However, only a fraction of the patients respond to ICB therapy. Accurate prediction of patients to likely respond to ICB would maximize the efficacy of ICB therapy. The tumor microenvironment (TME) dictates tumor progression and therapy outcome. Here, we classify the TME by analyzing the transcriptome from 11,069 cancer patients based on angiogenesis and T-cell activity. We find three distinct angio-immune TME subtypes conserved across 30 non-hematological cancers. There is a clear inverse relationship between angiogenesis and anti-tumor immunity in TME. Remarkably, patients displaying TME with low angiogenesis with strong anti-tumor immunity show the most significant responses to ICB therapy in four cancers. Re-evaluation of the renal cell carcinoma clinical trials provides compelling evidence that the baseline angio-immune state is robustly predictive of ICB responses. This study offers a rationale for incorporating baseline angio-immune scores for future ICB treatment strategies.</p>
Immune checkpoint molecule TIGIT regulates kidney T cell functions and mediates acute kidney injury
<p>This dataset includes the single cell RNA-seq data associated with the publication listed in the title (abstract below).<br> <br> CellRanger.zip contains the raw transcript counts as produced by CellRanger. There is one folder per sample. The samples are indicated by the folder name (e.g. KO_Ctrl). <br> <br> We have also included .h5ad files that contain of cells that passed quality control, as described in the manuscript.<br> <br> adTIGIT_raw_031422.h5ad contains all passing cells and the raw counts, as well as cell annotations ('celltype')<br> <br> adTIGIT_Tonly_091421.h5ad contains only T cells, .X contains the normalized data and T-cell sub-type ('cluster').<br> <br> Abstract: T cells mediate pathologic and reparative processes during acute kidney injury (AKI) but exact mechanisms regulating kidney T cell functions are unclear. This study identified upregulation of the novel immune checkpoint molecule, TIGIT, on mouse and human kidney T cells following AKI. TIGIT-expressing kidney T cells produced proinflammatory cytokines and had effector and central memory phenotype. Kidney Tregs were predominantly TIGIT+ and reduced after ischemia reperfusion (IR) injury. TIGIT deficient mice had protection from both ischemic and nephrotoxic AKI. Single cell RNA sequencing led to discovery of possible downstream targets of TIGIT. TIGIT mediates AKI pathophysiology, is a promising target for developing AKI therapy, and is being increasingly studied in human cancer therapy trials.</p>
OSE2101 Versus Chemotherapy in HLA-A2 Positive Patients With Advanced NSCLC After Immune Checkpoint Inhibitor Failure
ClinicalTrials.gov study NCT02654587. IPD Sharing: NO. Countries: 10. Publications: 1.
Conserved angio-immune subtypes of the cancer microenvironment predict response to immune checkpoint blockade therapy
Open the record for dataset details and reuse information.
Pretreatment Neutrophil-to-Lymphocyte Ratio, Mutational Load, and Outcomes in Patients Treated with Immune Checkpoint Inhibitors
<p>This dataset has been used to analyze the association between pre-treatment neutrophil-to-lymphocyte ratio and tumour mutational burden with survival and response to treatment in immunotherapy-treated patients with cancer. The dataset contains clinical and genomic data for 2,037 patients with 18 cancer types.</p>
Response to immune checkpoint blockade improved in pre-clinical model of breast cancer after bariatric surgery
<p>Bariatric surgery is becoming more prevalent as a sustainable weight loss approach, with vertical sleeve gastrectomy (VSG) being the first line of surgical intervention. We and others have shown that obesity exacerbates tumor growth while diet-induced weight loss impairs obesity-driven progression. It remains unknown how bariatric surgery-induced weight loss impacts cancer progression or alters responses to therapy. Using a pre-clinical model of diet induced obesity followed by VSG or diet-induced weight loss, breast cancer progression and immune checkpoint blockade therapy was investigated. Weight loss by bariatric surgery or weight matched dietary intervention before tumor engraftment protected against obesity-exacerbated tumor progression. However, VSG was not as effective as dietary intervention in reducing tumor burden despite achieving similar extent of weight and adiposity loss. Circulating leptin did not associate with changes in tumor burden. Uniquely, tumors in mice that received VSG displayed elevated inflammation and checkpoint ligand PD-L1. Further, mice that received VSG had reduced tumor infiltrating T lymphocytes suggesting an ineffective anti-tumor microenvironment. VSG-associated elevation of PD-L1 prompted us to next investigate the efficacy of immune checkpoint inhibitors in lean, obese, and formerly obese mice that lost weight by VSG or weight matched controls. While obese mice were resistant to immunotherapy, anti-PD-L1 potently impaired tumor progression after VSG through improved anti-tumor immunity. Thus, in formerly obese mice, surgical weight loss followed by immunotherapy reduced breast cancer burden. Further studies are necessary to determine how bariatric surgery sensitizes tumors to immune checkpoint inhibition.</p>
An ssGSEA Based Immune-related Gene Prognostic Signature Combining Immune Infiltration and Immune Checkpoint for Breast Cancer Patients
<p>This is the gene expression and related clinical data of breast cancer patients obtained from TCGA. Original codes and data from GEO database could be found in GitHub via link "https://github.com/Grevilblois/R-codes-for-manuscript".</p>
A machine learning model reveals expansive downregulation of ligand-receptor interactions enhancing lymphocyte infiltration in melanoma with developed resistance to Immune Checkpoint Blockade
<p>Data repository containing the data to reproduce the results and findings that are published in:</p> <p>Sahni, S., Wang, B., Wu, D. <em>et al.</em> A machine learning model reveals expansive downregulation of ligand-receptor interactions that enhance lymphocyte infiltration in melanoma with developed resistance to immune checkpoint blockade. <em>Nat Commun</em> <strong>15</strong>, 8867 (2024). https://doi.org/10.1038/s41467-024-52555-4</p>
Innate immune activation by checkpoint inhibition in patient-derived lung cancer tissues
<p><span>Although Pembrolizumab-based immunotherapy has significantly improved lung cancer patient survival, many patients show variable efficacy and resistance development. A better understanding of the drug's action is needed to improve patient outcomes. Functional heterogeneity of the tumor microenvironment (TME) is crucial to modulating drug resistance; understanding of individual patients' TME that impacts drug response is hampered by lack of appropriate models. </span></p> <p><span>Lung organotypic tissue slice cultures (OTC) with patients' native TME procured from primary and brain-metastasized (BM) non-small cell lung cancer (NSCLC) patients were treated with Pembrolizumab and/or beta-glucan (WGP, an innate immune activator). Metabolic tracing with<sup> 13</sup>C<sub>6</sub>-Glc/<sup>13</sup>C<sub>5,</sub><sup>15</sup>N<sub>2</sub>-Gln, multiplex immunofluorescence (mIF), and digital spatial profiling (DSP) were employed to interrogate metabolic and functional responses to Pembrolizumab and/or WGP.</span></p> <p><span>Primary and BM PD-1<sup>+</sup> lung cancer OTC responded to Pembrolizumab and Pembrolizumab + WGP treatments, respectively. Pembrolizumab activated innate immune metabolism and functions in primary OTC, which were accompanied by tissue damage. DSP analysis indicated an overall decrease in immunosuppressive macrophages and T cells but revealed microheterogeneity in immune responses and tissue damage. Two TMEs with altered cancer cell properties showed resistance. Pembrolizumab or WGP alone had negligible effects on BM-lung cancer OTC but Pembrolizumab + WGP blocked central metabolism with increased pro-inflammatory effector release and tissue damage.</span></p> <p><span>In depth metabolic analysis and multiplex TME imaging of lung cancer OTC demonstrated overall innate immune activation by Pembrolizumab but heterogeneous responses in the native TME of a patient with primary NSCLC. Metabolic and functional analysis also revealed synergistic action of Pembrolizumab and WGP in OTC of metastatic NSCLC.</span></p>
Combined tumor and immune signals from genomes or transcriptomes predict outcomes of checkpoint inhibition in melanoma
<p>Code and data for manuscript "Combined tumor and immune signals from genomes or transcriptomes predict outcomes of checkpoint inhibition in melanoma"</p>
Immune selection determines tumor antigenicity and influences response to checkpoint inhibitors
<p>R markdown files and source data to reproduce figures from the manuscript "Immune selection determines tumor antigenicity and influences response to checkpoint inhibitors"</p>
Immune selection determines tumor antigenicity and influences response to checkpoint inhibitors - Dataset
<p>Dataset used from the publication "Tumor and Microenvironment Evolution during Immunotherapy with Nivolumab" published in </p> <p>Cell. 2017 Nov 2;171(4):934-949.e16.</p> <p> doi: 10.1016/j.cell.2017.09.028. Epub 2017 Oct 12.</p>
Hepatotoxicity in immune checkpoint inhibitors: A pharmacovigilance study from 2014–2021
<p><span>Adverse events(AEs) related to hepatotoxicity have been reported in patients treated with immune checkpoint inhibitors (ICIs). As the number of adverse events increases, it is necessary to assess the differences in each immune checkpoint inhibitor regimen. The purpose of this study was to examine the relationship between ICIs and hepatotoxicity in a scientific and systematic manner. Data were obtained from the FDA Adverse Event Reporting System database (FAERS) and included data from the first quarter of 2014 to the fourth quarter of 2021. Disproportionality analysis assessed the association between drugs and adverse reactions based on the reporting odds ratio (ROR) and information components (IC). 9,806 liver adverse events were reported in the FAERS database. A strong signal was detected in older patients (≥65 years) associated with ICIs. Hepatic adverse events were most frequently reported with Nivolumab (36.17%). Abnormal liver function, hepatitis, and autoimmune hepatitis were most frequently reported, and hepatitis and immune-mediated hepatitis signals were generated in all regimens. In clinical use, patients should be alert to these adverse effects, especially in elderly patients, who may be aggravated by the use of ICI.</span></p>
The entanglement of extracellular matrix molecules and immune checkpoint inhibitors in cancer: a systematic review of the literature
<p><strong>The datasets include the results obtained upon a literature search on different databases: Web of science, Scopus and Pubmed.</strong></p> <p>The combination of mesh terms searched in the databases were “extracellular matrix molecules” or “extracellular matrix remodeling” and “immune checkpoint inhibitors” or “immunotherapy”.</p>
Personalizing Immune Checkpoint Inhibitor Therapy
ClinicalTrials.gov study NCT03409341. IPD Sharing: YES. Countries: 1. Publications: 6.
Arginase Inhibitor INCB001158 as a Single Agent and in Combination With Immune Checkpoint Therapy in Patients With Advanced/Metastatic Solid Tumors
ClinicalTrials.gov study NCT02903914. IPD Sharing: NO. Countries: 4. Publications: 2.
Quad Shot Radiotherapy in Combination With Immune Checkpoint Inhibition
ClinicalTrials.gov study NCT04454489. IPD Sharing: NO. Countries: 1. Publications: 1.
Immune-checkpoint Inhibitors and Surrogate Endpoints in Cancer Trials (SURROGATE-ICI)
ClinicalTrials.gov study NCT03963518. IPD Sharing: NO. Countries: 1. Publications: 2.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.