GEO DataSets

(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:

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

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) In our previous study, we identified global genetic and epigenetic aberrations in the tumors of oral squamous cell carcinoma (OSCC) patients who were habitual smokers. We hypothesized that cigarette smoke might play a role in oral malignant transformation. DOK cell line is a dysplasitc oral keratinocyte derived from a heavy smoker with OSCC. The differentially expressed genes between DOK and normal human oral keratinocytes (HOK) may provide important information about OSCC carcinogenesis mediated by cigarette smoking.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

4 Samples

Download data: TXT

(Submitter supplied) According to epidemiological studies, a vast majority, approximately 80%~90% of male OSCC patients in Taiwan habitually drink alcohol (A), and chew betel quid (B), and use cigarette (C). To assess the impact of these dietary factors on the epigenome, we conduct a high-throughput screen survey in an oral cancer cohort with exposure of A, B, and C. Results indicate aberrent methylation patterns are prevalent in OSCC patients with ABC risk factors.

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL8490

80 Samples

Download data: TXT

(Submitter supplied) From ~1,700 non-small cell lung cancer specimens collected at the MD Anderson Cancer Center over the years 1997 to 2005, we selected 914 tumors with detailed clinical and pathological information. We extracted RNA and DNA from frozen tissues using histology quality control from 700 cases. RNA was examined for quality using Agilent Bioanalyzer and RNA integrity number (RIN) was obtained for all specimens. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6884

275 Samples

Download data: TXT

(Submitter supplied) We have developed cdk4/hTERT-immortalized normal human bronchial epithelial cells (HBECs) to study lung cancer pathogenesis. By studying the oncogenic effect of common lung cancer alterations (p53, KRAS, and c-MYC) we demonstrate the ability of this model to characterize the stepwise transformation of bronchial epithelial cells to full malignancy. Using HBECs derived from multiple individuals we found: 1) the combination of five genetic alterations (p53, KRASV12, c-MYC, CDK4 and hTERT) is sufficient for full tumorigenic conversion of HBECs; 2) high levels of KRASV12 are required for full malignant transformation of HBECs, however these levels also stimulate oncogene-induced senescence; 3) RAS-induced senescence is largely bypassed with loss of p53 function; 4) over-expression of c-MYC greatly enhances malignancy but only in the context of sh-p53+KRASV12; 5) HBECs from different individuals vary in their sensitivity to transformation by these oncogenic manipulations; 6) serum-induced epithelial-to-mesenchymal transition (EMT) increases in vivo tumorigenicity; 7) genetically-identical clones of transformed HBECs exhibit pronounced differences in tumor growth, histology, and differentiation as well as sensitivity to standard platinum-based chemotherapies; and 8) an mRNA signature derived from tumorigenic and non-tumorigenic clones is predictive of outcome in lung cancer patients. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

15 Samples

Download data: TXT

(Submitter supplied) MicroRNAs are critical mediators of stem cell pluripotency, differentiation and malignancy. Limited information exists regarding microRNA alterations that facilitate initiation and progression of human lung cancers. In this study, array techniques were used to evaluate microRNA expression in normal human respiratory epithelia and lung cancer cells cultured in the presence or absence of cigarette smoke condensate (CSC). more...

Organism:

Homo sapiens

Type:

Other

Platform:

GPL16382

8 Samples

Download data: TXT

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

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL18635 GPL19057

12 Samples

Download data: BW

(Submitter supplied) Although abnormal nuclear structure is an important criterion for cancer diagnostics, remarkably little is known about its relationship to tumor development. Here we report that loss of lamin B1, a determinant of nuclear architecture, plays a key role in lung cancer. We found that lamin B1 levels were reduced in lung cancer patients. Lamin B1 silencing in lung epithelial cells promoted epithelial-mesenchymal transition, cell migration, tumor growth and metastasis. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18635

4 Samples

Download data: BW, XLSX

(Submitter supplied) Although abnormal nuclear structure is an important criterion for cancer diagnostics, remarkably little is known about its relationship to tumor development. Here we report that loss of lamin B1, a determinant of nuclear architecture, plays a key role in lung cancer. We found that lamin B1 levels were reduced in lung cancer patients. Lamin B1 silencing in lung epithelial cells promoted epithelial-mesenchymal transition, cell migration, tumor growth and metastasis. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: BW

(Submitter supplied) Polycomb repressive complexes (PRC) are frequently implicated in human cancer acting either as oncogenes or tumor suppressors. Here we show that PRC2 is a critical regulator of Kras-driven non-small-cell lung cancer (NSCLC) progression. Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances Kras-driven adenomagenesis and inflammation, respectively. Eed-loss-driven inflammation leads to massive macrophage recruitment and marked decline in tissue function. more...

Organism:

Homo sapiens; Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL13112 GPL17021 GPL16791

31 Samples

Download data: BED, BIGWIG, BW, TXT

(Submitter supplied) The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 480,000 CpGs in a total of 96 samples, including 8 hyperplasias, 33 endometrial cancers and 53 metastases, as well as 2 cell-lines.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL16304

96 Samples

Download data: IDAT

(Submitter supplied) Chronic low dose inorganic arsenic (iAs) exposure leads to changes in gene expression and epithelial-to-mesenchymal transformation. During this transformation, cells adopt a fibroblast-like phenotype accompanied by profound gene expression changes. While many mechanisms have been implicated in this transformation, studies that focus on the role of epigenetic alterations in this process are just emerging. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL17585 GPL17586

8 Samples

Download data: CEL, CHP

(Submitter supplied) To examine the global impact of iAs on DNA methylation patterns. Genomic DNA was Bisulfite converted and analyzed using Mini methly-seq.

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platforms:

GPL11154 GPL18460

4 Samples

Download data: BIGBED

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

Organism:

Homo sapiens

Type:

Methylation profiling by array; Expression profiling by array

Platforms:

GPL6884 GPL8490

289 Samples

Download data

(Submitter supplied) The independent population of lung adenocarcinoma and adjacent non-tumor lung used for verification of the EDRN/Canary Foundation study

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL8490

55 Samples

Download data: TXT