Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans

PROVIDER: PRJNA1144457 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30043300_1.fastq.gz	Fastqsanger.gz
	SRR30043300_2.fastq.gz	Fastqsanger.gz
	SRR30043301_1.fastq.gz	Fastqsanger.gz
	SRR30043301_2.fastq.gz	Fastqsanger.gz
	SRR30043302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 146

Similar Datasets

Mus musculus

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans

| PRJNA1144395 | ENA

Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans.

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans.

| PRJNA1146388 | ENA

Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (Visium).

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (Visium).

| PRJNA1142005 | ENA

Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq II).

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq II).

| PRJNA1142006 | ENA

Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq I).

Project description:Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans (RNA-Seq I).

| PRJNA1142004 | ENA

PLT012, a humanized CD36-blocking antibody, is effective for unleashing anti-tumor immunity against liver cancer and liver metastasis

Project description:Tumor cells develop various strategies to evade immune surveillance, one of which is the modulation of the metabolic state of the tumor microenvironment (TME). In response to metabolic stress in the TME, several tumor-infiltrating immune subsets upregulate CD36 to take up lipids. This leads to impaired anti-tumor immunity, as intratumoral regulatory T cells (Tregs) exhibit increased survival and suppressive activity, while CD8+ T cells become more susceptible to ferroptosis and exhaustion. Here, we develop a humanized anti-CD36 IgG4 antibody, PLT012, against the lipid-binding domain of CD36 with excellent safety and favorable pharmacokinetic features in mice and cynomolgus monkey. PLT012 alone or in combination with PD-L1 blockade or standard-of-care immunotherapy results in robust anti-tumor immunity in both immunotherapy-sensitive and -resistant hepatocellular carcinomas (HCCs). Notably, PLT012 also reprograms immune landscape of human HCC ex vivo. Our findings provide proof-of-concept evidence that PLT012 effectively reprograms anti-tumor immunity in HCC, positioning it as a first-in-class immunotherapy targeting CD36.

2025-04-11 | GSE291964 | GEO

Tumor and gut biopsies from refractory metastatic melanoma patients before and after treatment with fecal microbiota transplantation (FMT) and anti-PD-1 re-induction (Baruch et al, Science 2020)

Project description:We performed a phase I clinical trial to assess the safety and feasibility of fecal microbiota transplantation (FMT) and re-induction of anti-PD-1 immunotherapy in patients with anti-PD-1-refractory metastatic melanoma. FMT donors were two metastatic melanoma patients who achieved a durable complete response. FMT recipient patients were metastatic melanoma patients who failed at least one anti-PD-1 line of treatment. Each recipient patient received FMT implants from only one of the two donors. FMT was conducted by both colonoscopy and oral ingestion of stool capsules, followed by anti-PD-1 re-treatment (Nivolumab, BMS). Recipient patients underwent pre- and post-treatment stool sampling, tissue biopsy of both gut and tumor, and total body imaging. Clinical responses were observed in three patients, including two partial responses and one complete response. Notably, treatment with FMT was associated with favorable changes in immune cell infiltrates and gene expression profiles in both the gut lamina propria and the tumor microenvironment.

2020-12-31 | GSE162436 | GEO

PTEN loss confers resistance to anti-PD-1 therapy in nonsmall cell lung cancer by increasing tumor infiltration of regulatory T cells

Project description:Immunotherapy resistance in non-small cell lung cancer (NSCLC) may be mediated by an immunosuppressive microenvironment, which can be shaped by the mutational landscape of the tumor. Here, we observed genetic alterations in the PTEN/PI3K/AKT/mTOR pathway and/or loss of PTEN expression in >25% NSCLC patients, with higher frequency in lung squamous carcinomas (LUSCs). Patients with PTEN-low tumors had higher levels of PD-L1 and PD-L2 and showed worse progression-free survival when treated with immunotherapy. Development of a Ptennull LUSC mouse model revealed that tumors with PTEN loss were refractory to antiPD-1, highly metastatic and fibrotic, and secreted TGF-β/CXCL10 to promote conversion of CD4+ lymphocytes into regulatory T cells (Tregs). Human and mouse PTEN-low tumors were enriched in Tregs and expressed higher levels of immunosuppressive genes. Importantly, treatment of mice bearing Pten-null tumors with TLR agonists and anti-TGF-β antibody aimed to alter this immunosuppressive microenvironment led to tumor rejection and immunological memory in 100% of mice. These results demonstrate that lack of PTEN causes immunotherapy resistance in LUSC by establishing an immunosuppressive tumor microenvironment that can be reversed therapeutically.

2023-06-30 | GSE233862 | GEO

Chemohormonal Therapy Remodels Prostate Cancer Immune Microenvironment and Enhances Checkpoint Inhibitor-based immunotherapy

Project description:Checkpoint blockade immunotherapy is a promising strategy in cancer treatment, depending on a favorable preexisting tumor immune microenvironment. However, prostate cancer is usually considered as an immune “cold” tumor with the poor immunogenic response and low density of tumor-infiltrating immune cells. This research uses samples from prostate cancer patients showing that docetaxel-based chemohormonal therapy reprograms the immune microenvironment and increases tumor-infiltrating T cells. Mechanistically, docetaxel treatment activates the cGAS/STING pathway and induces the type I interferon signaling, which may boost T cell-mediated immune response. In a murine prostate cancer model, chemohormonal therapy sensitizes tumor-bearing mice to PD1-blockade therapy. These findings demonstrate that docetaxel-based chemohormonal therapy activates prostate cancer immunogenicity and acts cooperatively with anti-PD-1 checkpoint blockade, providing a combination immunotherapy strategy that would lead to better therapeutic benefit for prostate cancer.

2022-08-01 | GSE193898 | GEO

Impact of PD-L1 overexpression on immune checkpoint inhibitor efficacy in triple-negative breast cancer using a 4T1 murine model.

Project description:Bulk RNA sequencing was performed to investigate transcriptomic changes in 4T1 tumors treated with anti-PD-L1 therapy. Tumors were derived from 4T1 control and PD-L1-overexpressing cells injected into mice, followed by IgG or anti-PD-L1 treatment. Gene expression analysis revealed distinct immune-related pathway alterations, with reduced immune activation in PD-L1-overexpressing tumors. Differentially expressed genes suggested an immunosuppressive tumor microenvironment, potentially contributing to resistance to anti-PD-L1 therapy. These findings provide insights into the molecular mechanisms underlying immune checkpoint inhibitor response in triple-negative breast cancer.

2025-03-28 | GSE292013 | 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