Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from AJ and C3H mouse lungs exposed to NNK

ABSTRACT: Identification of genes associated with exposure to the carcinogen Nitrosamine (NNK) in mouse lungs of susceptible (AJ) and resistant (C3H) strains. Microarrays were used to capture all of the up and down regulated genes in two strains of mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE38952 | GEO | 2012/09/01

SECONDARY ACCESSION(S): PRJNA169369

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from AJ and C3H mouse lungs exposed to NNK

Project description:Identification of genes associated with exposure to the carcinogen Nitrosamine (NNK) in mouse lungs of susceptible and resistant strains. Microarrays were used to capture all of the up and down regulated genes in two strains of mice. Lungs were excised and analyzed between 3-12 weeks after exposure to NNK before mature tumors had formed

2012-09-01 | E-GEOD-38952 | biostudies-arrayexpress

Transcriptional responses to NNK and selenocystine in mouse lungs.

Project description:This study evaluated transcriptional effects of the lung carcinogen NNK ( 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) injection and selenocystine consumption on the murine lung. Female A/J mice at 5 weeks of age were obtained from The Jackson Laboratory. Animals were stabilized on an unsupplemented AIN-76 diet for one week prior to being given the selenium supplemented diet. The basal level of selenium in the diet is 0.35 ppm Se, the selenocytine supplemention was at 15 ppm. NNK was administered i.p. as a single 10 uM injection in 0.2 mL saline. With this protocol, 100% of animals reproducibly develop lung tumors after 3 months. Three days after NNK administration, animals were provided AIN-76A diets supplemented with selenocystine at 15 ppm selenium ad libitum for 10 days. Animals were sacrificed thirteen days after NNK administration. Lung tissue was harvested, immediately homogenized in Trizol and frozen. The organic extracted RNAs were run over Qiagen RNeasy columes before quantifying and qualifying them. All samples had RNA quality index's greater than 9. Four groups of A/J mice were utilized with 4 biological replicates per group. 1) Untreated - controls on the AIN-76 diet (0.35 ppm Se). 2) NNK treated - single injection of NNK, maintained on norma AIN-76 diet, sacraficed after 13 days. 3) SECY - selenocystine supplemented (15 ppm) for 10 days on a AIN-76 diet then sacraficed. 4) NNK plus SECY - single injection of NNK, after 3 days, selenocystine supplemented (15 ppm) diet for 10 days then sacraficed. RNAs from the the four untreated mice were combined to phenotypically anchor the dual color expression profile. mouse lung responses to NNK injection and/or selenocystine dietary supplementation

2012-05-31 | E-GEOD-29447 | biostudies-arrayexpress

Transcriptional responses to NNK and selenocystine in mouse lungs.

2012-06-01 | GSE29447 | GEO

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

Chimeric RNA RRM2-C2orf48 plays an oncogenic role in the development of NNK-induced lung cancer

Project description:Chimeric RNAs have been used as biomarkers and therapeutic targets for multiple types of cancers. However, less attention has been paid to their mechanism of action in neoplasia. Here, we report that chimeric RNA RRM2-C2orf48 promotes 4-(methyl nitrosamine)-1-(3-pyridinyl)-1-butanone (NNK)-induced lung cancer. We found that RRM2-C2orf48 had higher expression levels in lung cancer cell lines and in lung cancer tissues from 74 patients than in normal cells and tissues, respectively. And its expression level was correlated with smoking. Next, we demonstrate that the expression level of RRM2-C2orf48 could increase after treatment with 200 mg/L NNK for 24 h. Overexpressing RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and promoted cell growth. Meanwhile, suppressing RRM2-C2orf48 inhibited cell growth. Finally, we identified miR-219a-2-3p as a potential target of RRM2-C2orf48. In summary, RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and miR-219a-2-3p may be involved in this process.

2022-11-19 | GSE217991 | GEO

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

Lungs from ovalbumen sensitized and challenged C3H mice

Project description:Profile of gene expression in lungs of ovalbumen sensitized and challenged C3H mice. Keywords = C3H, lung, ovalbumen, mouse, Mus musculus, mice Keywords: parallel sample

2003-06-10 | GSE446 | GEO

Mus musculus

Project description:Expression data from AJ and C3H mouse lungs exposed to NNK

| PRJNA169369 | 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

C57BL/6 C3H/HeJ apoE-/- mice - gene expression in aorta

Project description:Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit a marked difference in their susceptibility to atherosclerosis and the arterial wall has proven to be a source of the difference in atherosclerosis susceptibility. Genome-wide gene expression analysis was conducted in aortic walls of the two strains. Total RNA was extracted from aortas of 6-week-old female B6 and C3H apoE-deficient (apoE-/-) mice fed a chow or Western diet. 1514 genes in chow fed mice and 590 genes in Western fed mice were found to be differentially expressed between the two strains. RNA was extracted from aorta using a Trizol protocol. Total RNA was pooled in an equal amount from 4 mice for each group. Standard Affymetrix procedures were performed using 8ug of total RNA. Microarrays were used to detect gene expression in aortic walls of two apoE-deficient mouse strains when fed a chow or western diet. Keywords: atherosclerosis, arterial walls, C57BL/6, C3H/HeJ, Inbred strains, Hyperlipidemia, and Western diet

2009-02-20 | GSE14854 | 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