Browse
Submit Data
Databases
API
Help

Dataset Information

7 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

WT1 Trio Peptide-vaccine for Rare Cancers

ABSTRACT: Interventions: A patient is vaccinated with Montanide ISA51-adjuvanted WT1 Trio cancer vaccine consisting of two WT1 CTL peptides (WT1-126 and WT1-235) and one WT1 HTL peptide (WT1-332) (2mg each) seven times at the interval of two weeks. Primary outcome(s): Induction of WT1-specific immune responses assessed by WT1-related tests such as WT1-DTH skin reaction and serum levels of WT1 peptide IgG autoantibody at 1M, 2M, and 3M of WT1 Trio vaccine. Study Design: Single arm Non-randomized

DISEASE(S): Thymic Cancer Thymoma Soft Tissue Sarcoma Malignant Glioma Salivary Gland Cancer Head And Neck Mucoepidermoid Carcinoma Olfactory Neuroblastoma Head And Neck Mucosal Malignant Melanoma Ophthalmic Malignant Melanoma Cancer Of The External Auditory Canal Testicular Cancer Cancer Of Penis Adrenal Cancer Malignant Mesothelioma Cancer Of The Small Intestine Merkel Cell Carcinoma Cutaneous Lymphoma (rare Cancers Listed Above)

PROVIDER: 2638832 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Long-term maintenance of anti-tumor immune responses by vaccination with tri-WT1 peptide cancer vaccine WT1 Trio

Project description:Interventions: A patient is vaccinated with Montanide ISA51-adjuvanted WT1 Trio cancer vaccine consisting of two WT1 CTL peptides (WT1-126 and WT1-235) and one WT1 HTL peptide (WT1-332) (2mg each) seven times at the interval of two to four weeks. The interval can be changed within a range from one to 16 weeks. Primary outcome(s): Induction of WT1-specific immune responses assessed by WT1-related tests such as WT1-DTH skin reaction, serum levels of WT1 peptide IgG autoantibody, and frequency of WT1-CTL in PB * This is evaluated at the interval ranging from 6 to 12 months. Study Design: Single arm Non-randomized

| 2638831 | ecrin-mdr-crc

Phase I Clinical trial of personalized peptide vaccine in combination with humanized anti-IL6 receptor monoclonal antibody for refractory colorectal cancer patients

Project description:Interventions: Anti-IL6 receptor antibody [Actemra (tocilizumab), Chugai Pharmaceutical Co; 0.5mg/kg (n=6), 2mg/kg (n=6), or 8mg/kg (n=6)] is intravenously administrated. After three days, a maximum of 4 peptides (3 mg/each peptide), which are selected based on the results of HLA typing and peptide-specific IgG titers, are subcutaneously administrated with incomplete Freund’s adjuvant (Montanide ISA51, Seppic)once a week for consecutive 6 weeks. During the treatment, safety is evaluated.The dose of anti-IL6 receptor antibody is escalated, if the safty is confirmed in 6 independent patients at the same dose. Primary outcome(s): Safety (adverse events) of personalized peptide vaccine in combination with anti-IL6 receptor antibody. Study Design: Single arm Non-randomized

| 2622910 | ecrin-mdr-crc

Genome wide WT1 binding sites in developing mouse kidneys

Project description:We report the the identification of chrosomal regions bound by the Wilms' tumor suppressor gene WT1 during embryonic mouse kidney development. Two indepednent ChIP-Seq experiments on microdissected E18.5 developing mouse kidneys were carried out using either WT1-specific or IgG-antibodies as a negative control.

2014-06-15 | E-GEOD-58179 | biostudies-arrayexpress

Influenza vaccination in the elderly boosts antibodies against conserved viral proteins and egg-produced glycans

Project description:Proteomic analysis of serum IgG antibody repertoire against influenza vaccine H1 (H1N1 A/California/7/2009) and H3 (H3N2 A/Texas/50/2012) in young, middle-aged, and elderly donors vaccinated with Fluzone 2013-14/14-15. Dataset consists of peak-response (days 21-28 post-vaccination) serum IgG samples eluted by affinity chromatography against H1 and H3 vaccine or hemagglutinin and the flow-throughs.

| MSV000086108 | MassIVE

Infant antibody repertoires during the first two years of influenza vaccination

Project description:Proteomic analysis of serum IgG antibody repertoire against influenza vaccine HAs in infant donors vaccinated with Fluzone 2017-18/18-19. Dataset consists of peak-response (days 14 and 21 post-vaccination) serum IgG samples eluted by affinity chromatography against IAV or IBV hemagglutinin and the flow-throughs.

2022-08-01 | MSV000090057 | MassIVE

mRNA expression profile of Lymphocytes by high-throuput sequencing

Project description:The activation of CD4+ T helper (Th) cells is crucial for the induction of cytotoxic T lymphocyte (CTL) responses against malignancy. We reprogrammed a Th clone specific for chronic myelogenous leukemia (CML)-derived b3a2 peptide to pluripotency and re-differentiated the cells into T-lineage cells (iPS-T cells). Although iPS-T cells retained the same T-cell receptor (TCR) as the original Th clone, their gene expression patterns resembled those of group 1 innate lymphoid cells, and CD4 molecule, an essential co-receptor in TCR-mediated Th responses, was not expressed. The transduction of CD4 genes into iPS-T cells enhanced b3a2 peptide–specific responses. iPS-T cells contained a subpopulation that up-regulates CD40 ligand (CD40L) in response to IL-2 and IL-15. Besides CD4 expression, CD40Lhigh iPS-T cells induced antigen-specific DC maturation characterized by enhanced CD83, CD86, and CCR7. In the presence of Wilms tumor 1 (WT1) peptide, DCs conditioned by CD4-modified CD40Lhigh iPS-T cells stimulated the priming of WT1-specific CTLs. These CTLs eliminated WT1 peptide-expressing CML cell lines in vitro and in vivo. Our findings indicate CD4 modification and purification of CD40Lhigh iPS-T cells generates T helper-like cells that induce effective anti-leukemic CTL responses via DC maturation and suggest feasibility of the cells for adoptive immunotherapy against leukemia.

2018-01-31 | GSE94332 | GEO

MEF-mKras-WT1

Project description:K-ras is one of the most frequently mutated human oncogenes. Activation of K-ras can lead to either senescence or proliferation in primary cells. The precise mechanism governing these distinct outcomes remains unclear. Here we utilized a loss-of-function screen to assess the role of specific genes identified as potential key regulators of K-ras driven oncogenesis. Using this approach, we identify the transcription factor Wt1 as an inhibitor of senescence in primary cells expressing oncogenic K-ras. Deletion or suppression of Wt1 expression leads to senescence of primary cells expressing oncogenic K-ras under the control of the native promotor at physiological levels, but has no effect on cells expressing wild-type K-ras. Wt1 contributes to K-ras driven lung tumorigenesis in vivo and loss of Wt1 is specifically deleterious to human lung cancer cell lines that are dependent on oncogenic K-ras. Taken together, these observations reveal a novel role for Wt1 as a key regulator of the complex genetic network required for the oncogenic effect of the small GTPase K-ras. We compare the expression profiles of Wild type, K-ras mutant, Wt1-null, and double K-ras mutant/Wt1-null mouse embryonic fibroblasts (MEFs). The study provides insights into the transcriptional role of Wt1 in the context of oncogenic K-ras.

2010-03-01 | GSE15325 | GEO

Passive Transfer of Vaccine-Elicited Antibodies Protects Against SIV in Rhesus Macaques

Project description:In this study, we show that passive transfer of purified antibodies from vaccinated macaques can protect naïve animals against SIVmac251 challenges. The protective signature included multiple antibody functions and correlated with upregulation of interferon pathways in the vaccinated animals. Adoptive transfer of purified IgG from the vaccinated animals with the most robust protective signatures provided partial protection against SIVmac251 challenges in naïve recipient rhesus macaques. These data demonstrate the protective efficacy of purified vaccine-elicited antiviral antibodies, even in the absence of virus neutralization.

2020-08-14 | GSE156177 | GEO

Transcription profiling of human WT1-mutant versus WT1 wild-type Wilms tumors

Project description:Gain-of-function mutations in exon 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant cases lack such "hot spot" mutations. To ask whether stabilization of beta-catenin might be essential after WT1 loss, and to identify downstream target genes, we compared expression profiles in WT1-mutant versus WT1 wild-type Wilms' tumors. Supervised and nonsupervised hierarchical clustering of the expression data separated these two classes of Wilms' tumor. The WT1-mutant tumors overexpressed genes encoding myogenic and other transcription factors (MOX2, LBX1, SIM2), signaling molecules (TGFB2, FST, BMP2A), extracellular Wnt inhibitors (WIF1, SFRP4), and known beta-catenin/TCF targets (FST, CSPG2, CMYC). Beta-Catenin/TCF target genes were overexpressed in the WT1-mutant tumors even in the absence of CTNNB1 exon 3 mutations, and complete sequencing revealed gain-of-function mutations elsewhere in the CTNNB1 gene in some of these tumors, increasing the overall mutation frequency to 75%. Lastly, we identified and validated a novel direct beta-catenin target gene, GAD1, among the WT1-mutant signature genes. These data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class. Beta-Catenin stabilization can initiate tumorigenesis in other systems, and this mechanism is likely critical in tumor formation after loss of WT1. Experiment Overall Design: Identification of WNT/Beta-Catenin or WT1 target genes. 39 individual samples.

2008-06-14 | E-GEOD-6120 | biostudies-arrayexpress

Studies in a murine B16 melanoma model show that persistent antigen at vaccination sites induces CD8+ T cell sequestration, dysfunction and deletion

Project description:To understand why cancer vaccine-induced T cells often fail to eradicate tumors, we studied immune responses in mice vaccinated with gp100 peptide emulsified in incomplete Freund's adjuvant (IFA), commonly used in clinical cancer vaccine trials. After gp100 peptide/IFA vaccination, tumor-specific CD8+ T cells (adoptively transferred from gp100-specific TCR-transgenic pmel-1 mice) accumulated not in tumors but at the persisting, antigen-rich vaccination site. Once there, primed T cells became dysfunctional and underwent antigen-driven, IFN-γ and FasL-mediated apoptosis, resulting in systemic hyporesponsiveness to subsequent vaccination. Provision of anti-CD40 antibody, TLR7 agonist and interleukin-2 (covax) reduced T cell apoptosis but did not prevent vaccination site sequestration. A non-persisting vaccine formulation shifted T cell localization towards tumors, inducing superior anti-tumor activity. Short-lived formulation also reduced systemic T cell dysfunction and promoted memory formation, as shown by gene expression profiling and other measures. Persisting peptide/IFA vaccine depots, currently used to vaccinate cancer patients, can induce specific T cell sequestration at vaccination sites followed by dysfunction and deletion; short-lived depot formulations may overcome these limitations and result in greater therapeutic efficacy of peptide-based cancer vaccines. To study the fate of melanoma-specific CD8+ T cells after peptide vaccination, we tracked T cell receptor-transgenic pmel-1 T cells in mice vaccinated with heteroclitic gp100_25-33 peptide emulsified in IFA. Splenic pmel-1 CD8+ T cells were purified at 6 and 21 days after vaccination with either gp100/IFA/covax or gp100/saline/covax, and then their total RNA was extracted and used for comparison by gene expression profiling.

2013-03-02 | E-GEOD-43929 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data