Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Integrated copy number and transcriptomic profiling reveal novel oncogenic drivers and clinically significant biomarkers in adenoid cystic carcinoma [Affymetrix]

ABSTRACT: This experiment investigates global gene expression in adenoid cystic carcinoma (30) and normal salivary gland tissue (7).

ORGANISM(S): Homo sapiens

PROVIDER: GSE153002 | GEO | 2023/08/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of adenoid cystic carcinoma (ACC) ACCX11 cells compared to normal salivary glands

Project description:PDX-derived ACCX11 adenoid cystic carcinoma cells were compared to normal salivary gland (NSG) controls.

2023-12-01 | E-MTAB-12978 | biostudies-arrayexpress

Integrated, genome-wide screening for hypomethylated oncogenes in salivary gland adenoid cystic carcinoma

2013-10-01 | GSE25746 | GEO

Xenograft model systems of adenoid cystic carcinoma

Project description:Adenoid cystic carcinoma (ACC) is one of the most common malignancies that arise in the salivary glands, with an incidence of 4.5 per 1,000,000. It can also arise in glandular tissue closely related to salivary glands in the lacrimal gland, nasal passages and tracheobronchial tree, as well as in glands of the breast and vulva. At all of these sites, it is characterized by a distinctive histology of basaloid epithelial cells arranged in cribriform or tubular patterns, usually demonstrating abundant hyaline extracellular matrix secretion and some degree of myoepithelial differentiation. ACC is generally a slow-growing tumor characterized by a protracted clinical course, usually well over 5 years in duration, marked by regional recurrence, distant metastasis and/or spread along peripheral nerves. A recurrent chromosomal translocation, t(6;9)(q23;p21), has been identified in ACC, and recently it has been discovered that in a majority of ACC the MYB gene on chromosome 6 is fused to the 3’ terminus of the NFIB gene on chromosome 9, creating a fusion gene product resulting in increased MYB-related transcriptional activation. Recently it has been determined that most cell lines with attribution of ACC derivation are either contaminants of other cell lines or do not have the characteristic MYB-NFIB translocation. Also, there are no animal models of this histologically and genetically defined tumor type. To address the paucity of experimental and pre-clinical models systems of ACC, we have for several years been establishing xenograft tumor lines from clinical samples of ACC. We describe our experience with these models and their characterization here. Analysis of 12 xenografts of human adenoid cystic carcinoma (ACC) along with 10 samples of ACC directly from humans. Note, that 12 of these samples are paired primary ACC & xenograft ACC from the same individual (6 pairs in total).

2011-05-03 | E-GEOD-28996 | biostudies-arrayexpress

Study the histone H3 lysine 9 trimethylation (H3K9me3) in adenoid cystic carcinoma cell lines (ACC) via ChIP-chip by array

Project description:Chromatin immunoprecipitation on microarrays (ChIP-chip) has been widely used to investigate the DNA binding sites for a variety of proteins such as histone and transcription factors on a genome-wide scale. The purpose of this study is to evaluate the status of histone H3 lysine 9 trimethylation in salivary gland adenoid cystic carcinoma.

2014-11-04 | E-MTAB-3053 | biostudies-arrayexpress

Spatial transcriptomics of adenoid cystic carcinoma of the lacrimal gland

Project description:We performed spatial transcriptomics of a tumor section from a patient post-treatment with adenoid cystic carcinoma of the lacrimal gland.

2023-07-05 | GSE228685 | GEO

Integrated, genome-wide screening for hypomethylated oncogenes in salivary gland adenoid cystic carcinoma

Project description:Salivary gland adenoid cystic carcinoma (ACC) is a rare malignancy amongst head and neck tumors that is poorly understood on a molecular level. We sought to perform a comprehensive approach for novel oncogene candidate screening under the control of promoter methylation in order to learn more about the molecular basis of this unusual disease. We performed global demethylation of normal salivary gland cell strains using 5-aza-deoxycytidine (5-Aza dC) and trichostatin (TSA). Expression arrays were performed, and the profiles of treated and untreated cells compared. We then used expression microarray analysis of primary ACC and normal salivary gland samples to generate ACC-specific expression profiling. Next, we integrated the two profiles to identify a subset of genes for further validation of decreased methylation in the promoter region in ACC vs normals. Finally, only genes that showed decreased methylation in ACC compared to normal were further validated for mRNA, protein, and promoter methylation levels in a larger ACC cohort.

2013-10-01 | E-GEOD-25746 | biostudies-arrayexpress

ChIP-seq of MYB in adenoid cystic carcinoma (ACC) ACCX11 cells

Project description:Chromatin immunoprecipitation was carried out using an anti-MYB antibody in PDX-derived ACCX11 adenoid cystic carcinoma cells. Input samples were extracted prior to the addition of antibody.

2023-12-01 | E-MTAB-12976 | biostudies-arrayexpress

Mutational characterization of adenoid cystic carcinoma

Project description:Mutational characterization of adenoid cystic carcinoma

| PRJNA197420 | ENA

Integrated copy number and transcriptomic profiling reveal novel oncogenic drivers and clinically significant biomarkers in adenoid cystic carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-02 | GSE153230 | GEO

Human adenoid cystic carcinoma vs. human normal lymphocyte

Project description:We analyzed ten adenoid cystic carcinomas of head and neck by array-based comparative genomic hybridization (a-CGH) using DNA chips spotted 4,030 BAC clones. After data smoothing by the adaptive weights smoothing (AWS) procedure with the gain and loss analysis of DNA (GLAD) algorithm, a total of 89 DNA copy number aberrations (DSCNAs) were detected. The frequent (≥30%) DSCNAs were loss of 6q24, 6q25, 8p23, 6q25, and 6q23 and gains of 6q23, 8p23, 9p11-13, and 22q13. High-level gain was detected on 12q12-15 including MDM2 in two cases. These two cases showed immunohistochemically positive status of MDM2 and negative status of p53 and p21. Furthermore, the total number of DSCNAs was significantly greater in ACC with loss of 6q than in other ACC, in ACC without loss of 8p23 than in other ACC, and in ACC with 8p23 gain than in ACC with 8p23 loss, respectively. Though there is a limit in the evidence, a-CGH detected several candidate chromosomal imbalances associated with DSCNA accumulation in ACC. 6q loss, 12q gain aCGH DNA copy number aberrations screening in human cancer adenoid cystic carcinoma (ACC).

2011-08-31 | E-GEOD-22328 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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