GEO DataSets

(Submitter supplied) Exposure to genotoxic stresses such as cosmic radiation and second-hand tobacco smoke may increase the risk of breast cancer formation. Towards an understanding of how exposure to these genotoxic agents affect breast cancer biogenesis, we have shown that treating non-tumorigenic immortalized breast MCF 10A cells with low doses (0.1 Gray) of radiation as well as cigarette smoke condensate can generate a neoplastic breast cancer phenotype. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

4 Samples

Download data: CEL, CHP

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Methylation profiling by array; Expression profiling by array

Platforms:

GPL8490 GPL4133

4 Samples

Download data: TXT

(Submitter supplied) Recent epidemiological studies demonstrate that both active and involuntary exposure to tobacco smoke increases the risk of breast cancer. Little is known, however, about the molecular mechanisms by which tobacco smoke contributes to breast carcinogenesis. To investigate these mechanisms we have analyzed gene expression and methylation in MCF 10A mammary epithelial cells chronically exposed to aqueous cigarette smoke extract (CSE).

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

2 Samples

Download data: TXT

(Submitter supplied) Recent epidemiological studies demonstrate that both active and involuntary exposure to tobacco smoke increases the risk of breast cancer. Little is known, however, about the molecular mechanisms by which tobacco smoke contributes to breast carcinogenesis. To investigate these mechanisms we have analyzed gene expression and methylation in MCF 10A mammary epithelial cells chronically exposed to aqueous cigarette smoke extract (CSE).

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL8490

2 Samples

Download data: TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

20 Samples

Download data: BED

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Other

Platforms:

GPL15520 GPL16791

10 Samples

Download data

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array; Expression profiling by array; Other; Genome binding/occupancy profiling by high throughput sequencing

4 related Platforms

86 Samples

Download data: BED, IDAT, PDF, TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10332

16 Samples

Download data: PDF, TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10332

9 Samples

Download data: PDF, TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL13534

31 Samples

Download data: IDAT, TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

53 Samples

Download data: CEL

(Submitter supplied) The study seeks to identify the epigenetic changes caused by exposure of to cigarette smoke condensate. To this goal human bronchial epithelial cells, BEAS-2B, were treated with 5-aza-2’deoxycitidine and trychostatin A (5AzaC/TSA) subsequent to a chronic exposure (1 month) to cigarette smoke condensate (CSC). As negative control served BEAS-2B cells that were untreated or treated with CSC/DMSO for one month without the subsequent application of 5Aza/TSA. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

17 Samples

Download data: CEL

(Submitter supplied) BEAS-2B cells have been treated with low doses (20µg/ml) of CSC for 4 months. As negative control BEAS-2B cells were treated with DMSO (the CSC solvent). Non-treated cells were cultivated in parallel. Keywords: time course, stress response

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

36 Samples

Download data: CEL

(Submitter supplied) It is well-described that the tumor stroma participates in cancer progression, but whether stromal factors can initiate breast tumorigenesis remains unclear. Using our previously described stromal-specific phosphatase and tensin homolog (PTEN) deletion mouse model, we investigated transformative events in young, non-tumor bearing animals. Here, we show stromal PTEN deletion initiates radiation-induced genomic instability on neighboring mammary epithelium through paracrine epidermal growth factor receptor (EGFR) activation. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL20775

6 Samples

Download data: CEL

(Submitter supplied) To understand tumorigenesis and cancer progression of mammary epithelium, we established a cell model combining over-expression of human telomerase reverse transcriptase gene (hTERT) and heavy-ion radiation from normal human mammary epithelial cells. We subsequently used RNA-seq method to acquire their transcriptomes from two characteristic cell lines, an immortal epithelial cell line (I_hMEC) and a tumorigenic epithelial cell line (T_hMEC), and to look for differentially expressed genes (DEGs) between immortalization and tumorigenicity. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL9442

2 Samples

Download data: TXT

(Submitter supplied) The goals of this study were to identify gene transcription changes in cells expressing activated H-RasV12 or activated versions of the ras effector domain mutants RasV12G37, RasV12S35, and RasV12C40 for the purpose of identifying common or unique transcription alterations in cells transformed by different ras signal transduction pathways. Keywords: genetic modification design

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL1528

16 Samples

Download data: GPR

(Submitter supplied) It is widely believed that the carcinogenic action of ionizing radiation is due to targeted DNA damage and resulting mutations, but there is also substantial evidence that non-targeted radiation effects alter epithelial phenotype and the stromal microenvironment. Activation of transforming growth factor β1 (TGFβ) is a non-targeted radiation effect that mediates cell fate decisions following DNA damage and regulates microenvironment composition; it could either suppress or promote cancer. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

65 Samples

Download data: CEL

(Submitter supplied) To identify m6A sites on endogenous nuclear RNAs, we performed miCLIP to identify m6A sites in PANC-1 cells. To identify NKAP binding sites on endogenous nuclear RNAs, we performed iCLIP for flag-tag NKAP to analyze the nuclear RNA binding with NKAP in the same cells.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20795

2 Samples

Download data: WIG

(Submitter supplied) Analysis of different expression of microRNAs in immortalized human pancreatic duct epithelial cells treated with cigarette smoke condensate. Cigarette smoking plays vital role in tumorigenesis and development of pancreatic ductal adenocarcinoma. Results provide insight in the machenisms involved in PDAC initiation and progression.

Organism:

Homo sapiens

Type:

Non-coding RNA profiling by array

Platform:

GPL20712

6 Samples

Download data: TXT

(Submitter supplied) Transforming growth factor beta-1 (TGFbeta) is a tumor suppressor during the initial stage of tumorigenesis, but it can switch to a tumor promoter during neoplastic progression. Ionizing radiation (IR), both a carcinogen and a therapeutic agent, induces TGFbeta activation in vivo. We now show that IR sensitizes human mammary epithelial cells (HMEC) to undergo TGFbeta-mediated epithelial to mesenchymal transition (EMT). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL3921

15 Samples

Download data: CEL, CHP