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863 results for “immune checkpoints”
Immune Checkpoint Inhibitor, Nivolumab, Combined with Chemotherapy Improved the Survival of Unresectable Ad-vanced and Metastatic Esophageal Squamous Cell Carcinoma: a real world experience
<p><strong>Figure S1 the detail of treatments.</strong> Blue arrow means this patient was still alive at the latest date of follow up. Hollow circle means this patient die. The others were lose follow up at the latest date of follow up.</p> <p><strong>Figure S2 progression free survival (PFS) of patients received immunotherapy, including 5 nivolumab and chemotherapy and 1 dual immune check point inhibitor, on different PD-L1 tumor cells (TC) expression.</strong> (A) divided by PD-L1 TC <1% or ≧1%. (B)divided by PD-L1 TC <10% or ≧10%.</p>
Combined immune checkpoint blockade increases myocardial secretion of H-FABP, NT-Pro-BNP, NLRP-3 inflammasome, Interleukin-1β and Interleukin-6: biochemical implications in cardio-immuno-oncology
<p>Background: Immune checkpoint inhibitors have transformed the treatment of several cancers by releasing restrained antitumor immune responses. Ipilimumab, an anti–cytotoxic T-lymphocyte–associated antigen 4 (CTLA-4) antibody, and nivolumab, an anti–programmed death-1 (PD-1) antibody, have individually improved survival in patients with melanoma, and their combination further enhances antitumor activity and survival. More recently, an anti-LAG3 human monoclonal antibody, Relatlimab, has been approved by FDA for combinatorial treatment with Nivolumab for metastatic melanoma and an anti-PD-L1 mAb,Atezolizumab, is undergoing clinical trials evaluation in combination with Ipilimumab for metastatic lung cancer.However,adverse events associated with these agents include dermatitis, endocrinopathies, colitis, hepatitis, and pneumonitis, which are all thought to arise from aberrant activation of autoreactive T cells. These toxic effects are more frequent and severe when immunomodulatory mAbs are used in combination. </p> <p>Methods: human cardiomyocytes co-cultured with hPBMC were exposed to monotherapy and combinatorial ICIs (PD-L1 and CTLA-4 or PD-1 and LAG-3 blocking agents, at 200 nM) for 48 h. After treatments, cardiac cell lysis and secretion of biomarkers of cardiotoxicity (H-FABP, NT-Pro-BNP), NLRP3-inflammasome and Interleukin 1 and 6 were determined through colorimetric and enzymatic assays. <strong>Results:</strong>Both Combinations of immune checkpoint inhibitors exertmore potent cardiotoxic side effects compared to monotherapies against human cardiac cells co-cultured with human lymphocytes. LDH release from cardiac cells was 43% higher in PDL-1/CTLA-4 blocking agents, and 35.7% higher in PD-1/LAG-3 blocking agents compared to monotherapies. Biomarkers of cardiotoxicity, such as H-FABP and NT-Pro-BNP were also strongly increased in combination therapy than monotherapies. NLRP3 inflammasome, IL-1β and IL-6 levels were also increased by PDL-1/CTLA-4 and PD-1/LAG-3 combined blocking agents compared to untreated cells and monotherapies. </p> <p><strong>Conclusions:</strong>Data of the present study, although in vitro, indicate that combinatorial immune checkpoint blockade on co-cultures of hPBMCs and cardiac cells, including for the first time the anti LAG-3 monoclonal antibody, induce a pro- inflammatory phenotype, thus indicating that these therapies should be closely monitored by the multidisciplinary team consisting of oncologists, cardiologists and immunologists.</p>
Germline Immunomodulatory Expression Quantitative Trait Loci (ieQTLs) Associated with Immune-Related Toxicity from Checkpoint Inhibition
<p>Robert Ferguson<sup>1,2,3*</sup>, Vylyny Chat<sup>1,2,3*</sup>, Leah Morales<sup>1,2,3</sup>, Danny Simpson<sup>1,2,3</sup>, Kelsey Monson<sup>1,2,3</sup>, Elisheva Cohen<sup>1,2,3</sup>,Sarah Zusin<sup>1,2,3</sup>, Gabriele Madonna<sup>4</sup>, Mariaelena Capone<sup>4</sup>, Ester Simeone<sup>4</sup>, Anna Pavlick<sup>5</sup>, Jason Luke<sup>6,7</sup>, Thomas F Gajewski<sup>8,9,10</sup>, Iman Osman<sup>1,3,11,12</sup>, Paolo Antonio Ascierto<sup>4</sup>, Jeffrey Weber<sup>1,3,11</sup>, Tomas Kirchhoff<sup>1,2,3</sup></p> <p>1Laura and Isaac Perlmutter Cancer Center, New York University Langone Health, New York, NY, USA<br> 2Departments of Population Health and Environmental Medicine, New York University- Grossman School of Medicine, New York, NY, USA<br> 3The Interdisciplinary Melanoma Cooperative Group, New York University-Grossman School of Medicine, New York, NY, USA<br> 4Melanoma Cancer Immunotherapy and Innovative Therapy Unit, Istituto Nazionale Tumori IRCCS Fondazione G. Pascale, Napoli, Italy<br> 5Division of Hematology & Medical Oncology, the Cutaneous Oncology Program, Weill Cornell Medicine and New York-Presbyterian, New York, USA<br> 6Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15213, USA.<br> 7UPMC Hillman Cancer Center, Pittsburgh, PA 15232, USA.<br> 8Department of Pathology, University of Chicago, Chicago, IL, USA.</p> <p>9Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL, USA.<br> 10Ben May Department for Cancer Research, University of Chicago, Chicago, IL, USA.<br> 11Department of Medicine, New York University-Grossman School of Medicine, New York, NY, USA<br> 12Ronald O. Perelman Department of Dermatology, New York University-Grossman School of Medicine, New York, NY, USA</p> <p>*These authors contributed equally to the work</p> <p>Corresponding author: Tomas Kirchhoff, PhD</p> <p><strong>ABSTRACT</strong><br> <strong>Background:</strong> Immune-checkpoint inhibition (ICI) has improved clinical outcomes for metastatic melanoma patients, however, 65-80% of patients treated with ICI experience immune-related adverse events (irAEs). Given the plausible link of irAEs with underlying host immunity, we explored if germline genetic variants controlling the expression of 42 immunomodulatory genes<br> were associated with the risk of irAEs in melanoma patients treated with the single-agent anti- CTLA-4 antibody ipilimumab (IPI).<br> <strong>Methods:</strong> We identified 42 immunomodulatory expression quantitative trait loci (ieQTLs) most significantly associated with the expression of 382 immune-related genes. These germline variants were genotyped in IPI-treated melanoma patients, collected as part of a multiinstitutional collaboration. We tested the association of ieQTLs with irAEs in a discovery cohort of 95 patients followed by validation in an additional 97 patients.<br> Results: We found that the alternate allele of rs7036417, a variant linked to increased expression of SYK, was strongly associated with an increased risk of grade 3-4 toxicity (OR= 7.46; 95% CI=2.65-21.03; p=1.43E-04). This variant was not associated with response (OR= 0.90; 95% CI=0.37-2.21; p=0.82).<br> Conclusion: We report that rs7036417 associates with increased risk of severe irAEs, independent of IPI efficacy. SYK plays an important role in B-cell/T-cell expansion and increased pSYK has been reported in patients with autoimmune disease. The association between rs7036417 and IPI irAEs in our data suggests a role of SYK over-expression in irAE development. These findings support the hypothesis that inherited variation in immune-related pathways modulate ICI toxicity and suggest SYK as a possible future target for therapies to reduce irAEs.</p> <p> </p> <p><strong>Keywords:</strong> irAEs; germline variants; immune checkpoint inhibition; melanoma</p> <p><strong>Funding:</strong> This research was funded by the Italian Ministry of Health (IT-MOH) through “Ricerca Corrente”, grants number M2/2 and L2-1.</p> <p> </p> <p> </p> <p> </p> <p> </p> <p> </p>
Data from: The CD73 immune checkpoint promotes tumor cell metabolic fitness
<p>CD73 is an ectonucleotidase overexpressed on tumor cells that suppresses anti-tumor immunity. Accordingly, several CD73 inhibitors are currently being evaluated in the clinic, including in large randomized clinical trials. Yet, the tumor cell-intrinsic impact of CD73 remains largely uncharacterized. Using metabolomics, we discovered that CD73 significantly enhances tumor cell mitochondrial respiration and aspartate biosynthesis. Importantly, rescuing aspartate biosynthesis was sufficient to restore proliferation of CD73-deficient tumors in immune-deficient mice. Seahorse analysis of a large panel of mouse and human tumor cells demonstrated that CD73 enhanced oxidative phosphorylation (OXPHOS) and glycolytic reserve. Targeting CD73 decreased tumor cell metabolic fitness, increased genomic instability and suppressed poly ADP ribose polymerase (PARP) activity. Our study thus uncovered an important immune-independent function for CD73 in promoting tumor cell metabolism and provides the rationale for previously unforeseen combination therapies incorporating CD73 inhibition.</p>
High risk clear cell renal cell carcinoma microenvironments contain protumour immunophenotypes lacking specific immune checkpoints.
<p>Final Seurat file (rds) produced from the immune cell analysis performed in "<strong>High risk clear cell renal cell carcinoma microenvironments contain protumour immunophenotypes lacking specific immune checkpoints</strong>.<em><strong>"</strong></em></p>
The Expression of Immune Checkpoint CD28 rs1980422-related Single-nucleotide Polymorphisms in the Primary Immune Thrombocytopenia
ClinicalTrials.gov study NCT05468866. IPD Sharing: YES. Countries: 1. Publications: 4.
Immune Checkpoint Inhibitor Response in Solid Tumors Using a Live Tumor Diagnostic Platform
ClinicalTrials.gov study NCT06349642. IPD Sharing: NO. Countries: 1. Publications: 1.
Immuno-pet IMaging ResPonses AdministeRed Immune CheckpoiNt InhibiTor
ClinicalTrials.gov study NCT06218069. IPD Sharing: NO. Countries: 2. Publications: 11.
Extensive CArdioVAscular Characterization and Follow-up of Patients Receiving Immune Checkpoint Inhibitors
ClinicalTrials.gov study NCT05699915. IPD Sharing: NO. Countries: 1. Publications: 1.
SJS/TEN or Other Cutaneous Adverse Eevents Induced by Immune Checkpoint Inhibitors (ICIs) vs. Non-ICIs
ClinicalTrials.gov study NCT06522048. IPD Sharing: NO. Countries: 1. Publications: 5.
Specific Biomarkers of Immune-mediated Hepatitis Secondary to Immune Checkpoint Inhibitors
ClinicalTrials.gov study NCT06470997. IPD Sharing: Not stated. Countries: 1. Publications: 9.
Immune Checkpoint Inhibitors and Atherosclerotic Plaque Volume
ClinicalTrials.gov study NCT04430712. IPD Sharing: Not stated. Countries: 1. Publications: 1.
LND101 for Fecal Microbiota Transplantation in Combination With Immune Checkpoint Blockade in Advanced Melanoma
ClinicalTrials.gov study NCT06623461. IPD Sharing: YES. Countries: 1. Publications: 1.
Influenza Vaccination in Patients Receiving Immune Checkpoint Inhibitor
ClinicalTrials.gov study NCT03590808. IPD Sharing: NO. Countries: 1. Publications: 9.
Phase II Study of Neoadjuvant Immune Checkpoint Inhibitor in Patients With Resectable Gastrointestinal Cancers
ClinicalTrials.gov study NCT04196465. IPD Sharing: Not stated. Countries: 1. Publications: 0.
JOint Use of Database to Identify Risk Factors of CARDio-vascular Toxicity Induced by Immune Checkpoint Inhibitors
ClinicalTrials.gov study NCT04294771. IPD Sharing: NO. Countries: 1. Publications: 7.
Immune Checkpoint Inhibition in Combination With Radiation Therapy in Pancreatic Cancer or Biliary Tract Cancer Patients
ClinicalTrials.gov study NCT02866383. IPD Sharing: NO. Countries: 1. Publications: 2.
Genetically Engineered Natural Killer (NK) Cells With or Without Atezolizumab for the Treatment of Non-small Cell Lung Cancer Previously Treated With PD-1 and/or PD-L1 Immune Checkpoint Inhibitors
ClinicalTrials.gov study NCT05334329. IPD Sharing: Not stated. Countries: 1. Publications: 2.
REduced Frequency ImmuNE Checkpoint Inhibition in Cancers
ClinicalTrials.gov study NCT04913025. IPD Sharing: NO. Countries: 1. Publications: 1.
Evaluation of the Role of Immune Checkpoints in Response to Breast Cancer Neoadjuvant Therapy
ClinicalTrials.gov study NCT05519397. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.
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Allen Brain Atlas
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
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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.