Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-sequencing of lung tissues from Gprc5a-/- mice at baseline, end of NNK exposure, three months and seven months post-NNK

ABSTRACT: RNA-sequencing of lung tissues from Gprc5a-/- mice at baseline, end of NNK exposure, three months and seven months post-NNK

PROVIDER: PRJNA613283 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

Project description:We have shown that Gprc5a-/- mice form Kras-mutant lung tumors spontaneously which is accelerated by tobacco carcinogen (NNK) exposure. We found in these mice that Lcn2 was distinctively up-regulated along the spectrum of Kras-mutant lung cancer development. To understand the role of Lcn2 in lung cancer pathogenesis, we generated Gprc5a-/-/Lcn2-/- mice and found that these animals have increased lung tumor devleopment following NNK compared to Gprc5a-/- animals with intact Lcn2. To understand these effects, we performed RNA-sequencing (RNA-Seq) of lung tissues from Gprc5a-/-/Lcn2-/- and Gprc5a-/- mice at baseline (prior to NNK exposure) and of tumor-bearing lungs from both groups at seven months post-NNK exposure.

2021-03-19 | GSE147148 | GEO

RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

Project description:RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

| PRJNA613199 | ENA

RNA-sequencing of lung tissues from Gprc5a-/- mice at baseline, end of NNK exposure, three months and seven months post-NNK

Project description:We have previously shown that Gprc5a-KO mice develop lung tumors that are accelerated by exposure to the tobacco-specific carcinogen NNK. In this study we sought to understand the temporal evolution of gene expression changes in tumors and normal-appearing tissues.

2021-03-31 | GSE147187 | GEO

Gene expression fluctuation in Abatacept treated Rheumatoid Arthritis patients between baseline and 6 months

Project description:The objective of this study was to identify response-specific gene expression fluctuations in methotrexate /abatacept (Aba) treated rheumatoid arthritis patients : responders (R) VS no-responders (NR). Nineteen RA patients were received Abatacept. The drug efficacy was evaluated with the DAS28 score after 6 months of treatment according to the EULAR response criteria. Among 19 Aba RA patients, 14 were R and 5 were classified as NR. A blood sample was carried out in patients both at baseline (just before the first injection of ABA) and at 6 months in PaxGene tubes.

2020-07-24 | GSE91079 | GEO

Differential gene expression patterns in lung carcinogenesis mediated by loss of mouse tumor supressor Gprc5a

Project description:Increasing the understanding of the impact of changes in oncogenes and tumor suppressor genes is essential for improving the management of lung cancer. Recently, we identified a new mouse lung-specific tumor suppressor - the G-protein coupled receptor 5A (Gprc5a). We sought to understand the molecular consequences of Gprc5a loss and towards this we performed microarray analysis of the transcriptomes of lung epithelial cells cultured from normal tracheas of Gprc5a knockout and wild-type mice to define a loss-of-Gprc5a gene signature. Moreover, we analyzed differential gene expression patterns between Gprc5a knockout normal lung epithelial cells as well as lung adenocarcinoma cells isolated and cultured from tumors of NNK-exposed Gprc5a knockout mice.

2010-04-13 | GSE21309 | GEO

RNA-sequencing of NNK-exposed Gprc5a-/- lung tumors

Project description:RNA-sequencing of NNK-exposed Gprc5a-/- lung tumors

| PRJNA421345 | ENA

Gene expression analysis of mouse Kras-mutant lung adenocarcinoma cells and cancer stem cells

Project description:Mechanisms underlying cancer stemness in Kras-mutant lung adenocarcinoma (KM-LUAD) are poorly understood. We previously found that mice with knockout of Gprc5a develop LUADs with somatic Kras mutations. We also previously derived Gprc5a-/- KM-LUAD cells (MDA-F471 cells) from a mouse exposed to the tobacco-specific carcinogen NNK. We also derived cancer stem cells (CSCs; grown and cultured as spheres in 3D cultures) from MDA-F471 cells. To better understand the biology of these CSCs, we compared the transcriptomes of MDA-F471 cells and their CSC counterparts by bulk RNA-sequencing.

2022-11-30 | GSE219124 | GEO

Baseline Expression of Inflammatory Cytokines and Receptors in Normal Breast Tissue and Seven Breast Cancer Cell Lines

Project description:Baseline Expression of Inflammatory Cytokines and Receptors in Normal Breast Tissue and Seven Breast Cancer Cell Lines

| PRJNA319559 | ENA

Temporal RNA-sequencing of cytologically-normal mouse airway epithelia during tobacco carcinogen-associated lung tumorigenesis

Project description:Smoking perpetuates in cytologically-normal airways a molecular “field of injury” that is pertinent to lung cancer and early detection. The evolution of airway field changes prior to lung cancer onset is poorly understood largely due to the long latency of lung malignancy in smokers. Here we studied airway expression changes prior to lung cancer onset in mice with knockout of the Gprc5a gene and tobacco carcinogen (nicotine-specific nitrosamine ketone; NNK) exposure and that develop the most common type of lung cancer, lung adenocarcinoma (LUAD). Cytologically-normal airway epithelial brushings were collected before exposure and at multiple times following NNK exposure until time of LUAD development and then analyzed by RNA-sequencing (RNA-Seq).

2020-02-28 | GSE102707 | GEO

Transcription profiling of human tumours at baseline and after 21 days of treatment with sorafenib and dacarbazine

Project description:Background New approaches are needed to improve prognostic accuracy for treatment response and to explore the complexities of drug effects on human tumours. We developed a strategy of global genomic investigation of sequential tumor biopsies at baseline and 21 days post-treatment, and applied this approach in a phase I study of sorafenib plus dacarbazine in patients with solid tumours. Methods 23 patients received 21-day cycles of oral sorafenib, 400 mg twice daily and dacarbazine, 1000 mg/m2 by 1-h intravenous infusion on day 1. Efficacy was assessed using response evaluation criteria in solid tumours. Differential gene expression was assessed through genomic microarray analysis of biopsy tissue from the same tumour at baseline and on day 21. Seven parameters characterizing vascularisation using dynamic enhanced-contrast ultrasonography (DCE-US) were assessed. Changes from baseline in the two parameters were characterized for patients with and without a clinical response to treatment at 3 months.Findings 23 patients were evaluable for efficacy and 17 for gene expression and DCE-US analyses. One patient had a partial response; 14 had stable disease. Genomic analyses identified a 247-gene signature that distinguished progressors from nonprogressors at 3 months. Expression of four genes was significantly associated with progression at 3 months. Functional parameters of DCE-US representing blood volume at baseline, day 8, and day 21 correlated with 3-month disease progression status.Interpretation This novel approach of sequential investigations in a phase I trial was feasible, detecting early changes in gene expression and tumour vascularity that may be predictive of clinical outcome.

2010-07-31 | E-TABM-760 | 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