Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Senescent fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity

ABSTRACT: Senescent fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity

PROVIDER: PRJNA1117434 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Senescent fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity

Project description:Our study identified a druggable component of the tumor stroma that fulfills the metabolic requirement of tumor cells to acquire a more aggressive phenotype.

2024-08-27 | GSE268478 | GEO

Assessing the plasticity of the senescent phenotype

Project description:Assessing the plasticity of the senescent phenotype

| PRJNA699010 | ENA

Senescent stroma mediates immunosuppression and drives breast cancer progression

Project description:Senescent stroma mediates immunosuppression and drives breast cancer progression

| PRJNA954051 | ENA

Senescent cancer-associated fibroblasts in pancreatic adenocarcinoma impair CD8+ T cell activation and limit responsiveness to immunotherapy in mice

Project description:Senescent cells within tumors and their stroma exert complex pro- and anti-tumorigenic functions, yet the potential for targeting such senescent cells for improved therapy remains largely unknown. Here, we uncover the presence of a senescent subset of cancer-associated fibroblasts (CAFs) within pancreatic ductal adenocarcinomas (PDAC) and in premalignant lesions in mice and humans. Senescent CAFs represented different previously-defined CAF subtypes. Senescent CAFs isolated from mouse and humans expressed elevated levels of immunoregulatory genes. Depletion of senescent CAFs, either genetically or using the Bcl-2 inhibitor ABT-199 (venetoclax), increased the proportion of activated CD8+ T cells in mouse pancreatic carcinomas, whereas induction of CAF senescence had the opposite effect. Combining ABT-199 with an immune checkpoint therapy regimen significantly reduced mouse tumor burden. These results indicate that senescent CAFs in PDAC stroma limit the numbers of activated cytotoxic CD8+ T cells, and suggest that their targeted elimination through senolytic treatment may enhance immunotherapy.

2024-06-24 | PXD053144 | Pride

Senescent stroma mediates immunosuppression and drives breast cancer progression [MMF]

Project description:Senescent stroma mediates immunosuppression and drives breast cancer progression [MMF]

| PRJNA954046 | ENA

Senescent stroma mediates immunosuppression and drives breast cancer progression [CAF]

Project description:Senescent stroma mediates immunosuppression and drives breast cancer progression [CAF]

| PRJNA954044 | ENA

Senescent cancer-associated fibroblasts in pancreatic adenocarcinoma suppress CD8+ T cell activation and inhibit response to immune checkpoint therapy [Cultured_Human_Mouse]

Project description:Senescent cells appear within tumors and their stroma, exerting complex pro- and anti-tumorigenic functions. The effects of senescent tumor stromal cells are mostly unknown, as is the potential for targeting such senescent cells for improved therapy. Here we uncover the presence of a senescent subset of cancer-associated fibroblasts (CAFs) within pancreatic adenocarcinomas and in premalignant pancreatic lesions. Senescent CAFs show reduced proliferation, and are often associated with the inflammatory CAF (iCAF) subtype. We isolated and characterized senescent CAFs from mouse models and directly from human patients, and found that they express elevated levels of immune-regulatory genes. In a panel of mouse PDACs, high levels of senescent CAFs correlated with low T cell infiltration. Removal of senescent CAFs from PDAC stroma, either genetically or through treatment with the senolytic drug ABT-199 (venetoclax), a Bcl2 inhibitor, increased rates of activated cytotoxic CD8+ T cells within tumors. Conversely, activation of CAF senescence within PDACs led to reduced CD8+ T cell numbers. Media from senescent PDAC CAFs inhibited T cell proliferation and activation. We show that implanted PDAC tumors show improved response to immune checkpoint therapy when co-treated with the senolytic drug. These results reveal that the presence of senescent CAFs in PDAC stroma acts to repress cytotoxic T cell activity, and suggest that their targeted elimination through senolytic treatment may enhance immunotherapy.

2024-06-06 | GSE235233 | GEO

Senescent cancer-associated fibroblasts in pancreatic adenocarcinoma suppress CD8+ T cell activation and inhibit response to immune checkpoint therapy [hPDAC]

2024-06-06 | GSE235244 | GEO

Senescent cancer-associated fibroblasts in pancreatic adenocarcinoma suppress CD8+ T cell activation and inhibit response to immune checkpoint therapy [Kras_p53]

2024-06-06 | GSE235242 | GEO

Senescent stroma mediates immunosuppression and drives breast cancer progression [scRNA-seq]

Project description:Senescent stroma mediates immunosuppression and drives breast cancer progression [scRNA-seq]

| PRJNA954052 | ENA