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254 results for “Tumor antigens”
Cross-reactive CD8+ T cell responses to tumor-associated antigens (TAAs) and homologous microbiota-derived antigens (MoAs)
<p><strong><span>Background: </span></strong><span>We have recently shown extensive sequence and conformational homology between tumor-associated antigens (TAAs) and antigens derived from microorganisms (MoAs). The present study aimed to assess the breadth of T-cell recognition specific to MoAs and the corresponding TAAs in healthy subjects (HS) and patients with cancer (CP).</span></p> <p><strong><span>Method: </span></strong><span>A library of >100 peptide-MHC (pMHC) combinations was used to generate DNA-barcode labelled multimers. Homologous peptides were selected from the Cancer Antigenic Peptide Database, as well as Bacteroidetes/Firmicutes-derived peptides. They were incubated with CD8+ T cells from the peripheral blood of HLA-A*02:01 healthy individuals (n=10) and cancer patients (n=16). T cell recognition was identified using tetramer-staining analysis. Cytotoxicity assay was performed using as target cells TAP-deficient T2 cells loaded with MoA or the paired TuA.</span></p> <p><strong><span>Results: </span></strong><span>A total of 66 unique pMHC recognized by CD8+ T cells across all groups were identified. Of these, 21 epitopes from microbiota were identified as novel immunological targets. Reactivity against selected TAAs was observed for both HS and CP. pMHC tetramer staining confirmed CD8+ T cell populations cross-reacting with CTA SSX2 and paired microbiota epitopes. Moreover, PBMCs activated with the MoA where shown to release IFNγ as well as to exert cytotoxic activity against cells presenting the paired TuA.</span></p> <p><strong><span>Conclusions: </span></strong><span>Several predicted microbiota-derived MoAs are recognized by T cells in HS and CP. Reactivity against TAAs was observed also in HS, primed by the homologous bacterial antigens. CD8+ T cells cross-reacting with MAGE-A1 and paired microbiota epitopes were identified in three subjects. Therefore, the microbiota can elicit an extensive repertoire of natural memory T cells to TAAs, possibly able to control tumor growth (“natural anti-cancer vaccination”). In addition, non-self MoAs can be included in preventive/therapeutic off-the-shelf cancer vaccines with more potent anti-tumor efficacy than those based on TAAs.</span></p>
MOLECULAR MIMICRY BETWEEN TUMOR ASSOCIATED ANTIGENS AND MICROBIOTA-DERIVED EPITOPES.
<p><strong>Background: </strong>The gut microbiota profile is unique for each individual and are composed by different bacteria species according to individual birth-to-infant transitions. In the last years, the local and systemic effects of microbiota on cancer onset, progression and response to treatments, such as immunotherapies, have been extensively described. Here we offer a new perspective, proposing a role for the microbiota based on the molecular mimicry of tumor-associated antigens by microbiome-associated antigens.</p> <p><strong>Methods:</strong> In the present study we looked for homology between published TAAs and non-self microbiota-derived epitopes. Blast search for sequence homology was combined with extensive bioinformatics analyses.</p> <p><strong>Results:</strong> Several evidences for homology between TAAs and microbiota-derived antigens have been found. Strikingly, three cases of 100% homology between the paired sequences has been identified. The predicted average affinity to HLA molecules of microbiota-derived antigens is very high (<100nM). The structural conformation of the microbiota-derived epitopes is, in general, highly similar to the corresponding TAA. In some cases, it is identical and contact areas with both HLA and TCR chains are indistinguishable. Moreover, the spatial conformation of TCR-facing residues can be identical in paired TAA and microbiota-derived epitopes, with exactly the same values of planar as well as dihedral angles.</p> <p><strong>Conclusions:</strong> The data reported in the present study show for the first time the high homology in the linear sequence as well as in structure and conformation between TAAs and peptides derived from microbiota species of the Firmicutes and the Bacteroidetes phyla, which together account for 90% of gut microbiota. Cross-reacting CD8<sup>+</sup> T cell responses are very likely induced. Therefore, the anti-microbiota T cell memory may turn out to be an anti-cancer T cell memory, able to control the growth of cancer developed during the lifetime if the expressed TAA is similar to the microbiota epitope. This may ultimately represent a relevant selective advantage for cancer patients and may lead to a novel preventive anti-cancer vaccine strategy.</p>
Pan-cancer Proteomics Analysis to Identify Tumor-Enriched and Highly Expressed Cell Surface Antigens as Potential Targets for Cancer Therapeutics
<p>CPTAC PAN-cancer Data Repository</p> <p>Welcome to the CPTAC PAN-cancer Data Repository! This repository serves as a data repository for the CPTAC PAN-cancer effort, which focuses on cancer target discovery. It contains various data sets related to protein abundance estimation, derived TMT-TPA, iBAQ, iBAQ-derived copy number, and differential protein expression for CPTAC ten indications.</p> <p>## Contents</p> <p>The repository includes the following data:</p> <p>- FragPipe Output: Protein abundance estimation data generated using the FragPipe software.<br> - Derived TMT-TPA: Data derived from Tandem Mass Tag (TMT) based Total Protein Approach (TPA).<br> - iBAQ: Data representing intensity-based absolute quantification (iBAQ) of proteins.<br> - iBAQ-derived Copy Number: Data derived from iBAQ analysis for copy number estimation.<br> - Differential Protein Expression: Data indicating differential expression of proteins between tumor and NAT.</p> <p>## Data Organization</p> <p>The data in this repository is organized in a structured manner to facilitate easy access and navigation. The repository structure is as follows:</p> <p>FragPipe/<br> [fragpipe_data_files]<br> Derived_TMT_TPA/<br> [derived_tmt_tpa_data_files]<br> iBAQ/<br> [ibaq_data_files]<br> iBAQ-derived_copy_number/<br> [ibaq_copy_number_data_files]<br> Differential_protein_expression/<br> [differential_expression_data_files]</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>
A Phase 1 Study of Mixed Bacteria Vaccine (MBV) in Patients With Tumors Expressing NY-ESO-1 Antigen
ClinicalTrials.gov study NCT00623831. IPD Sharing: YES. Countries: 1. Publications: 1.
Human Leukocyte Antigen-A*02:01-restricted Tumor Vessel Specific Peptide Vaccination for Advanced Pancreatic Cancer
ClinicalTrials.gov study NCT00683085. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Relationship Between Tumor Mutation Burden and Predicted Neo-antigen Burden in Patients With Advanced Melanoma or Bladder Cancer Treated With Nivolumab or Nivolumab Plus Ipilimumab (CA209-260)
ClinicalTrials.gov study NCT02553642. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Non-coding regions are the main source of targetable tumor-specific antigens - DATASETS (k=24)
<p>Tumor-specific antigens (TSAs) represent ideal targets for cancer immunotherapy, but few have been identified thus far. We therefore developed a proteogenomic approach to enable the high-throughput discovery of TSAs coded by potentially all genomic regions. In two murine cancer cell lines and seven human primary tumors, we identified a total of 40 TSAs, about 90% of which derived from allegedly non-coding regions and would have been missed by standard exome-based approaches. Moreover, the majority of these TSAs derived from non-mutated yet aberrantly expressed transcripts (such as endogenous retroelements) that could be shared by multiple tumor types. In mice, the efficacy of TSA vaccination was influenced by two parameters that can be estimated in humans and could serve for TSA prioritization in clinical studies: TSA expression and the frequency of TSA-responsive T cells in the pre-immune repertoire. In conclusion, the strategy reported herein could considerably facilitate the identification and prioritization of actionable human TSAs.</p>
Non-coding regions are the main source of targetable tumor-specific antigens – DATASETS (k=33)
<p>Tumor-specific antigens (TSAs) represent ideal targets for cancer immunotherapy, but few have been identified thus far. We therefore developed a proteogenomic approach to enable the high-throughput discovery of TSAs coded by potentially all genomic regions. In two murine cancer cell lines and seven human primary tumors, we identified a total of 40 TSAs, about 90% of which derived from allegedly non-coding regions and would have been missed by standard exome-based approaches. Moreover, the majority of these TSAs derived from non-mutated yet aberrantly expressed transcripts (such as endogenous retroelements) that could be shared by multiple tumor types. In mice, the efficacy of TSA vaccination was influenced by two parameters that can be estimated in humans and could serve for TSA prioritization in clinical studies: TSA expression and the frequency of TSA-responsive T cells in the pre-immune repertoire. In conclusion, the strategy reported herein could considerably facilitate the identification and prioritization of actionable human TSAs.</p>
A Phase I Trial of T Cells Expressing an Anti-GD2 Chimeric Antigen Receptor in Children and Young Adults With GD2+ Solid Tumors
ClinicalTrials.gov study NCT02107963. IPD Sharing: YES. Countries: 1. Publications: 4.
A Study of ADXS-NEO Expressing Personalized Tumor Antigens
ClinicalTrials.gov study NCT03265080. IPD Sharing: NO. Countries: 1. Publications: 0.
Immunotherapy of Melanoma With Tumor Antigen RNA and Small Inhibitory RNA Transfected Autologous Dendritic Cells
ClinicalTrials.gov study NCT00672542. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Tumor Associated Antigen Specific T Cells (TAA-T) With PD1 Inhibitor for Lymphoma
ClinicalTrials.gov study NCT03843294. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Clinical Study of Redirected Autologous T Cells With a Chimeric Antigen Receptor in Patients With Malignant Tumors
ClinicalTrials.gov study NCT03302403. IPD Sharing: NO. Countries: 1. Publications: 1.
Analysis of the Incidence of Expression of Tumor Antigens in Pathologically Proven Stage I, II and III Non-Small Cell Lung Cancer(NSCLC) in Asiatic Patients
ClinicalTrials.gov study NCT01837511. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Immunotherapy Using Precision T Cells Specific to Personalized Neo-antigen for the Treatment of Advanced Malignant Tumor of Biliary Tract
ClinicalTrials.gov study NCT02632019. IPD Sharing: Not stated. Countries: 1. Publications: 43.
Incidence of Expression of Tumor Antigens in Cancer Tissue From Patients With Pathologically Demonstrated Bladder Cancer
ClinicalTrials.gov study NCT01706185. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Human Leukocyte Antigen-A*2402-Restricted Tumor Vessel Specific Peptide Vaccination for Advanced Pancreatic Cancer
ClinicalTrials.gov study NCT00683358. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Immunotherapy Using Precision T Cells Specific to Multiple Common Tumor-Associated Antigen Combined With Transcatheter Arterial Chemoembolization for the Treatment of Advanced Hepatocellular Carcinoma
ClinicalTrials.gov study NCT02638857. IPD Sharing: Not stated. Countries: 1. Publications: 25.
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International Brain Laboratory public data
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OpenNeuro
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