Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas

ABSTRACT: Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas

PROVIDER: PRJNA931755 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [RNA-Seq]

Project description:Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [RNA-Seq]

| PRJNA934450 | ENA

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [Cut&Tag]

Project description:Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [Cut&Tag]

| PRJNA865693 | ENA

Spontaneously evolved progenitor niches escape Yap oncogene addiction in advanced pancreatic ductal adenocarcinomas.

Project description:Lineage plasticity has been proposed as a major source of intratumoral heterogeneity and therapeutic resistance. Here, by employing an inducible genetic engineered mouse model, we illustrate that lineage plasticity enables advanced Pancreatic Ductal Adenocarcinoma (PDAC) tumors to develop spontaneous relapse following elimination of the central oncogenic driver - Yap. Transcriptomic and immunohistochemistry analysis of a large panel of PDAC tumors reveals that within high-grade tumors, small niches of PDAC cells gradually evolve to re-activate pluripotent transcription factors (PTFs), which lessen their dependency on Yap. Comprehensive Cut&Tag analysis demonstrate that although acquisition of PTF expression is coupled with the process of epithelial-to-mesenchymal transition (EMT), PTFs form a core transcriptional regulatory circuitry (CRC) with Jun to overcome Yap dependency, which is distinct from the classic TGFb-induced EMT-TF network. A chemical-genetic screen and follow-up functional studies establish Brd4 as an epigenetic gatekeeper for the PTF-Jun CRC, and strong synergy between BET and Yap inhibitors in blocking PDAC growth.

| S-EPMC10017707 | biostudies-literature

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [RNA-Seq]

Project description:Lineage plasticity has been proposed as a major source of intratumoral heterogeneity and therapeutic resistance. Employing an inducible genetic engineered mouse model, we illustrate that lineage plasticity enables advanced Pancreatic Ductal Adenocarcinoma (PDAC) tumors to develop spontaneous relapse following elimination of the central oncogenic driver - Yap. Transcriptomic and immunohistochemistry analysis of a large panel of PDAC tumors reveals that within high-grade tumors, small niches of PDAC cells gradually evolve to re-activate pluripotent transcription factors (PTFs), which lessen their dependency on Yap. Comprehensive Cut&Tag analysis demonstrate that although acquisition of PTF expression is coupled with the process of epithelial-to-mesenchymal transition (EMT), PTFs form a core transcriptional regulatory circuitry (CRC) with Jun to overcome Yap dependency, which is distinct from the classic TGFb-induced EMT-TF network. A chemical-genetic screen and follow-up functional studies establish Brd4 as an epigenetic gatekeeper for the PTF-Jun CRC, and strong synergy between BET and Yap inhibitors in blocking PDAC growth.

2023-03-02 | GSE224566 | GEO

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [Cut&Tag]

2023-01-11 | GSE210412 | GEO

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-02-06 | GSE224567 | GEO

Mature tertiary lymphoid structures are key niches of tumor-specific immune responses in pancreatic ductal adenocarcinomas

Project description:Mature tertiary lymphoid structures are key niches of tumor-specific immune responses in pancreatic ductal adenocarcinomas

| PRJNA941867 | ENA

Downregulation of anti-inflammatory A20 promotes immune escape of lung adenocarcinomas

Project description:We found that the potent anti-inflammatory enzyme A20 is a potent tumor suppressor and hence often downregulated in human and mouse lung adenocarcinoma. Comparison of gene expression profiles of A20 expressing versus A20 deficient lung tumor tissue samples revealed that loss of A20 enhanced the cellular response to interferons. This hypersensitivity to interferons was responsible to drive immune evasion of A20 deficient lung adenocarcinomas. ,

2021-04-01 | GSE148194 | GEO

Transcriptomes of lung adenocarcinomas

Project description:Transcriptomes of lung adenocarcinomas

| PRJNA638137 | ENA

Transcriptomes of lung adenocarcinomas

Project description:Transcriptomes of lung adenocarcinomas

| PRJNA593979 | ENA