450k Analysis of 24 HNSCC cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Matthias Lechner
PROVIDER: E-GEOD-38270 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2012-11-30 | E-GEOD-38271 | biostudies-arrayexpress
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
2012-11-30 | E-GEOD-38266 | biostudies-arrayexpress
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: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
2012-11-30 | E-GEOD-38268 | biostudies-arrayexpress
Project description:The life cycle of human papillomaviruses (HPV) is strictly linked to the differentiation of their natural host cells. The HPV E6 and E7 oncoproteins can delay the normal differentiation program of keratinocytes, however, the exact mechanisms responsible for this have not yet been identified. The goal of this study was to investigate the effects of HPV16 oncoproteins on the expression of genes involved in keratinocyte differentiation. Primary human keratinocytes transduced by LXSN (control) retroviruses or virus vectors expressing HPV16 E6, E7 or E6/E7 genes were subjected to gene expression profiling. The results of microarray analysis showed that HPV 16 E6 and E7 have the capacity to down-regulate the expression of several genes involved in keratinocyte differentiation. Quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed to confirm microarray data. To investigate the effects of the HPV oncoproteins on the promoters of selected keratinocyte differentiation genes, luciferase reporter assays were performed. Our results suggest that the HPV 16 E6 and/or E7 oncogenes are able to down-regulate the expression of several genes involved in keratinocyte differentiation, at least partially by down-regulating their promoter activity. This activity of the HPV oncoproteins may have a role in the productive virus life cycle, and also in virus induced carcinogenesis. Primary human foreskin keratinocytes were transduced by retrovirus vectors containing HPV 16 E6, E7, E6/E7 or the control vector LXSN. The global gene expression patterns of transduced keratinocytes were analyzed on Affymetrix microarrays
2014-06-26 | E-GEOD-58841 | biostudies-arrayexpress
Project description:The analysis of the 6 methylomes by MeDIP-Seq comprise 3 HPV+ HNSCC samples and 3 HPV- HNSCC samples Analysis of the 6 methylomes, comprising 3 HPV+ HNSCC samples and 3 HPV- HNSCC samples
2012-11-01 | E-GEOD-38263 | biostudies-arrayexpress
Project description:ABSTRACT Two major subgroups of head and neck squamous cell carcinomas (HNSCC) are currently distinguished based on etiology and pattern of genetic alterations; tumors with biologically active human papillomavirus (HPV) and tumors without. It is at present unclear whether additional genetically distinct subgroups exist within HPV-negative HNSCC. Aim of this study is to genetically classify HNSCC without HPV involvement and to correlate the genetically defined classes to tumor and patient characteristics. By means of array comparative genomic hybridization (aCGH) we determined DNA copy number variation in thirty-nine HPV-negative, but further unselected HNSCC. Unsupervised analysis of aCGH data distinguished two genetic groups in HPV-negative HNSCC, one characterized by a low level of chromosomal alterations (N=9), and another by a high level of chromosomal alterations (N=30). Absence of chromosomal aberrations was significantly associated with wild-type TP53, a low level of alcohol consumption, a female gender and a better prognosis. The tumors were negative for microsatellite instability. The discovery of this new class of HNSCC with unique genetic and clinical characteristics has important consequences for future basic and clinical studies. All DNAs are isolated from fresh frozen HNSCC specimen. All tissue specimens were microdissected to obtain at least 90% tumor DNA. All sampels are hybridized against a pool of reference DNA of normal individuals of the opposite gender.
2009-03-11 | E-GEOD-11929 | biostudies-arrayexpress
Project description:Oncogenic human papillomaviruses (HPVs) are associated with nearly all carcinomas of the uterine cervix and have also become an increasingly important factor in the etiology of a subset of oropharyngeal tumors. HPV-associated head and neck cancers (HNSCCs) have a distinct risk profile and appreciate a prognostic advantage compared to HPV-negative HNSCC. We analyzed the genome-wide expression patterns in two HPV(+) and two HPV(-) squamous cell carcinoma (SCC) cell lines. The Affymetrix Human Genome U133 Plus 2.0 Array platform was used to assess genome-wide expression differences between the HPV(+) and HPV(-) cell lines utilizing the RMA normalization package available for R. Cell lines analyzed: UM-SCC-4, UM-SCC-47, UM-SCC-74A, and CaSki.
2010-12-01 | E-GEOD-24089 | biostudies-arrayexpress
Project description:Oncogene expressing human papillomavirus type 16 (HPV16) is found in a subset of head and neck squamous cell carcinomas (HNSCC). HPV16 drives carcinogenesis by inactivating p53 and pRb with the viral oncoproteins E6 and E7, reflected by a low level of mutations in TP53 and allelic loss at 3p, 9p and 17p, genetic changes frequently found in HNSCCs of non-viral etiology. We hypothesize that two pathways to HNSCC exist: one determined by HPV16 and one by environmental carcinogens. To define the critical genetic events in these two pathways, we now present a detailed genome analysis of HNSCC with and without HPV16 involvement by employing high resolution micro-array comparative genomic hybridization. Four regions showed alterations in HPV-negative tumors that were absent in HPV-positive tumors: losses at 3p11.2-26.3, 5q11.2-35.2, 9p21.1-24, and gains/amplifications at 11q12.1-13.4. Also, HPV16-negative tumors demonstrated loss at 18q12.1-23, in contrast to gain in HPV16-positive tumors. Seven regions were altered at high frequency (>33%) in both groups: gains at 3q22.2-qter, 5p15.2-pter, 8p11.2-qter, 9q22-34.1, 20p-20q and losses at 11q14.1-qter and 13q11-33. These data show that HNSCC arising by environmental carcinogens are characterized by genetic alterations that differ from those observed in HPV16-induced HNSCC, and most likely occur early in carcinogenesis. A number of genetic changes are shared in both tumor groups and can be considered crucial in the later stages of HNSCC progression. Tumor DNA is isolated from fresh frozen tissue. Tumor DNA is enriched by microdissection. Reference DNA is isolated from blood of normal individuals of the opposit gender.
2009-05-26 | E-GEOD-11931 | biostudies-arrayexpress
Project description:Inflammatory skin diseases, including inflammatory linear verrucous epidermal naevus (ILVEN) and psoriasis, are known to collectively be hyperproliferative. We endeavoured to do a transcriptional comparative study on patient and control keratinocytes to uncover a final druggable common pathway for those disorders.
2023-09-01 | E-MTAB-12925 | biostudies-arrayexpress