Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Whole transcriptome sequencing data of GBSCC patients from India

ABSTRACT: Our study has elucidated the immunoregulatory gene expression landscape in primary tumors of Gingivo-Buccal Squamous Cell Carcinoma, as compared to their adjacent normal tissue and computationally estimated a relative composition of various immune cell classes in those tissues. A detailed portrayal of expression variation of immune evasion genes alongwith other potential therapeutic targets have been highlighted in the study.

ORGANISM(S): Homo sapiens

PROVIDER: GSE101547 | GEO | 2017/09/27

SECONDARY ACCESSION(S): PRJNA394765

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Histone methylation antagonism drives tumor immune evasion in squamous cell carcinomas

Project description:Histone methylation antagonism drives tumor immune evasion in squamous cell carcinomas

| PRJNA773062 | ENA

Intestinal helminth skews dendritic cell development to counter the anti-helminth immune response

Project description:Intestinal dendritic cells (DC) orchestrate the adaptive immune response that balances protection against pathogens and tolerance towards harmless antigens. Yet, it remains largely unknown what molecular mechanisms underly this functional duality. Heligmosomoides polygyrus bakeri (Hpb) is a naturally occurring parasite in mice characterised by unique immune-evasion strategies that counter host protective immunity. Here, we utilised this unique infection environment to study mechanisms by which DC maintain the immune balance. In-depth characterisation of intestinal DC during Hpb infection revealed the emergence of distinct populations of DC that drive protective Th2 responses, versus others with immunoregulatory properties. We also identified that the skewing of intestinal DC towards immunoregulatory functions was due to TGFb signalling via endogenous sources or by Hpb-produced TGFb-mimic molecules. Thus, our results present a mechanistic explanation for Hpb’s ability to modulate the adaptive immune system. Furthermore, these data offer an example of how heterogeneity within the DC compartment can determine the simultaneous generation of both pro- and anti-inflammatory immune responses.

2025-03-17 | GSE291087 | GEO

Targeting IGF2BP1 reverses immune evasion in CTL-enriched pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) remains poorly responsive to immune checkpoint therapy. To investigate tumor-intrinsic immune evasion mechanisms, we performed RNA-sequencing of the basal-like PANC-03.27 PDAC cell line following IGF2BP1 knockdown using pooled siRNAs. Transcriptome profiling revealed induction of interferon-γ signaling and downregulation of curated IGF2BP1 target transcripts, consistent with a conserved immunoregulatory program. Gene set enrichment analysis and STAT reporter assays confirmed activation of JAK/STAT-dependent pathways. These datasets provide a resource for understanding IGF2BP1-mediated transcriptional regulation in PDAC and for identifying potential targets to enhance anti-tumor immune responses.

2026-02-11 | GSE319148 | GEO

Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion

Project description:Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion

| PRJNA883199 | ENA

Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [scRNAseq]

Project description:Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [scRNAseq]

| PRJNA883203 | ENA

Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [bulkRNAseq]

Project description:Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [bulkRNAseq]

| PRJNA882909 | ENA

GNPS - Metabolomics data for Figure 1D-1F. Schofield et al, Cell Reports,

Project description:Metabolomics raw LCMS files for Figure 1D-1F. Schofield et al, Cell Reports, "Acod1 Expression in Cancer Cells Promotes Immune Evasion through the Generation of Inhibitory Peptides".

2024-03-03 | MSV000094226 | GNPS

Inhibition of PGE2-EP2/EP4 signaling elicits anti-tumor immunity through reprograming of inflammatory myeloid cells and suppression of mRegDC-Treg axis

Project description:The discovery of immune checkpoint inhibitor (ICI) has highlighted the clinical importance of immune evasion in cancer. However, only a fraction of cancer patients show response to ICI, raising a question on immune suppression mechanisms other than immune checkpoint. In this study, we examined the role of the lipid inflammatory mediator PGE2 in immune evasion of the ICI-insensitive Lewis Lung Carcinoma line 1 (LLC1) mouse model. Inhibition of PGE receptors, EP2 and EP4, significantly suppressed tumor growth through the modulation of host immune cells. Single cell RNA-sequencing analysis revealed that EP2/4 inhibition elicited anti-tumor immunity through the reprogramming of inflammatory myeloid cells by downregulating expression of genes in NFB signaling and actions and suppression of the mregDC-regulatory T cell axis by downregulating genes associated with regulatory T cell recruitment and activation. Taken together, our work suggests that PGE2-EP2/EP4 signaling induces proinflammatory myeloid and tolerogenic lymphoid environments in ICI-insensitive tumors, which is amenable to EP2 and EP4 inhibitors..

2022-06-14 | GSE169688 | GEO

CGRP signaling Links Tumor-Associated Pain to Immune Evasion in Oral Squamous Cell Carcinoma

Project description:CGRP signaling Links Tumor-Associated Pain to Immune Evasion in Oral Squamous Cell Carcinoma

| PRJNA1399335 | ENA

Gene expression data from mouse squamous cell carcinoma cells

Project description:We describe a function of focal adhesion kinase (FAK) in driving anti-tumor immune evasion. The kinase activity of nuclear-targeted FAK in squamous cancer cells drives exhaustion of CD8+ T-cells and recruitment of regulatory T-cells by transcriptionally regulating chemokine/cytokine and ligand-receptor networks, including transcription of Ccl5 that is crucial. These changes inhibit antigen-primed cytotoxic CD8+ T-cell activity, permitting growth of FAK-expressing tumors. To address how FAK activity in squamous cell carcinoma (SCC) cancer cells promotes elevated intra-tumoral regulatory T-cells, we analyzed global transcriptional profiles of SCC cells expressing or not expressing FAK.

2015-09-29 | GSE71662 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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