450k Analysis of 24 HNSCC cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE38270 | GEO | 2012/11/30
SECONDARY ACCESSION(S): PRJNA167713
REPOSITORIES: GEO
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Project description:The methylation analysis of HPV+ HNSCC cell lines and HPV- HNSCC cell lines as well as clones from an infected HPV- cell line by Infinium HumanMethylation450 BeadChip Analysis of 24 450k methylation profiles, comprising 3 HPV+ HNSCC cell lines and 3 HPV- HNSCC cell lines (in duplicate each) and 12 infected HPV- HNSCC cell line clones
2012-11-30 | E-GEOD-38270 | biostudies-arrayexpress
Project description:The methylation analysis of 21 FFPE HPV+ HNSCC samples and 21 FPPE HPV- HNSCC samples by Infinium HumanMethylation450 BeadChip
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Project description:The methylation analysis of 21 FFPE HPV+ HNSCC samples and 21 FPPE HPV- HNSCC samples by Infinium HumanMethylation450 BeadChip Analysis of 42 450k methylation profiles, comprising 21 HPV+ HNSCC samples and 21 HPV- HNSCC samples
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Project description:The methylation analysis of 3 FF HPV+ HNSCC samples and 21 FP HPV- HNSCC samples by Infinium HumanMethylation450 BeadChip Analysis of 6 450k methylation profiles, comprising 3 HPV+ HNSCC samples and 3 HPV- HNSCC samples
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Project description:Genome wide DNA methylation profiling of HPV positive and HPV negative head and neck squamous cell cancer (HNSCC) samples. The Illumina Infinium 450k Human DNA methylation Beadchip v1.1 was used to obtain DNA methylation profiles across approximately 485577 CpGs in 4 HPV positive and 4 HPV negative HNSCC tumors
2015-03-21 | GSE67114 | GEO
Project description:Human papillomavirus (HPV)-associated head and neck cancers (HNSCCs) have a distinct risk profile and appreciate a prognostic advantage compared to HPV-negative HNSCC. Promoter hypermethylation has been widely recognized as an important mechanism in the progression of HNSCC, but the extent to which this mechanism is consistent between HPV(+) and HPV(-) tumors is unknown. To assess the genome-wide methylation changes in HPV(+) and HPV(-) tumors, we analyzed DNA methylation and expression patterns in two HPV(+) and two HPV(-) cell lines. HPV(+) tumors have overall higher DNA methylation in genic and LINE1 regions than HPV(-) tumors, and polycomb repressive complex 2 (PRC2) targets tend to be much more highly methylated in HPV(+) cells. Bisulphite-converted DNA from 4 squamous cell carcinoma (SCC) cell lines were hybridized to the Illumina Infinium 27k Human Methylation Beadchip.
2010-12-01 | E-GEOD-24087 | biostudies-arrayexpress
Project description:Human cancer cell lines are the most frequently used preclinical models in the study of cancer biology and the development of therapeutics. Although anatomically diverse, human papillomavirus (HPV)-driven cancers have a common etiology and similar mutations that overlap with but are distinct from those found in HPV-negative cancers. Building on prior studies that have characterized subsets of head and neck squamous cell carcinoma (HNSCC) and cervical squamous cell carcinoma (CESC) cell lines separately, we performed genomic, viral gene expression, and viral integration analyses on 74 cell lines that include all readily-available HPV-positive (9 HNSCC, 8 CESC) and CESC (8 HPV-positive, 2 HPV-negative) cell lines and 55 HPV-negative HNSCC cell lines. We used over 700 human tumors for comparison. Mutation patterns in the cell lines were similar to those of human tumors. We confirmed HPV viral protein and mRNA expression in the HPV-positive cell lines. We found HPV types in three CESC cell lines that are distinct from those previously reported. We found that cell lines and tumors had similar patterns of viral gene expression; there were few sites of recurrent HPV integration. As seen in tumors, HPV integration did appear to alter host gene expression in cell lines. The HPV-positive cell lines had higher levels of p16 and lower levels of Rb protein expression than did the HPV-negative lines. Although the number of HPV-positive cell lines is limited, our results suggest that these cell lines represent suitable models for studying HNSCC and CESC, both of which are common and lethal.
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Project description:The involvement of microRNAs (miRNAs) in cancer and their potential as biomarkers of diagnosis, prognosis and response to therapy is becoming increasingly appreciated. The etiology of head and neck squamous cell carcinoma (HNSCC) is predominantly associated with the synergistic effects of tobacco and alcohol use, as well as Human Papilloma Virus (HPV) infection, which embodies a distinct clinical and biological phenotype. We sought to examine whether the profile of miRNAs in HNSCC varies based on HPV status, and to identify specific miRNAs altered in head and neck carcinogenesis. Total RNA was isolated from 16 HNSCC fresh frozen primary tumors, 5 fresh frozen non-diseased head and neck epithelial tissues, and 2 HNSCC cell lines. The miRNA profile of 662 individual miRNAs in these tissues was examined by microarray. 18 miRNAs are significantly altered in their expression between normal tissues and HNSCC tumors and 5 miRNAs are identified as significantly differentially expressed between HPV-positive (HPV+) and HPV-negative (HPV-) tumors. A striking difference in expression pattern of miRNA was also observed between primary tissues and cell lines. These data suggest that the pattern of miRNA expression may be reflective of disease etiology, and may be useful in the realm of diagnostic biomarkers defining broadly responsive prevention and treatment strategies for HNSCC. These data also suggest that cultured tumor cell lines may be inappropriate for novel miRNA biomarker identification. Keywords: miRNA; Disease-state analysis Expression of 662 individual miRNA was assessed in16 HNSCC fresh frozen primary tumors, 5 fresh frozen non-diseased head and neck epithelial tissues, and 2 HNSCC cell lines were arrayed
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Project description:We report the first RNA-Seq experiments profiling the effects of DEK loss in HNSCC. Our data also incorporates HPV+ and HPV- tumors to idenfity HPV-dependent and -independent gene signatures. RNA-Seq of DEK-dependent gene signatures in HNSCC cell lines
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