Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1049986 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27209700_1.fastq.gz | Fastqsanger.gz | |||
| SRR27209700_2.fastq.gz | Fastqsanger.gz | |||
| SRR27209701_1.fastq.gz | Fastqsanger.gz | |||
| SRR27209701_2.fastq.gz | Fastqsanger.gz | |||
| SRR27209702_1.fastq.gz | Fastqsanger.gz |
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Project description:Adenoid cystic carcinoma (ACC) is an uncommon malignant neoplasm (incidence of 0.35 per 100,000) that occurs in different body sites. It most often arises in salivary glands and other secretory glands in the head and neck region. To find the gene expression signatures of ACC, we performed microarray experiments to compare ACC xenograft tumor models and normal tissue samples. We used microarrays to detail the global program of gene expression underlying adenoid cystic carcinoma and identified distinct classes of up- and down-regulated genes compared to non-neoplastic salivary tissue.
2012-03-27 | GSE36820 | GEO
Project description:Sox4 is upregulated in adenoid cystic carcinoma (ACC). The ACC3 cell line is the most widely available cell culture model system of this tumor type. RNAi mediated knockdown of Sox4 in ACC3 cells induces apoptosis.
2007-10-02 | E-GEOD-4225 | biostudies-arrayexpress
Project description:Adenoid cystic carcinoma (ACC) is an uncommon malignant neoplasm (incidence of 0.35 per 100,000) that occurs in different body sites. It most often arises in salivary glands and other secretory glands in the head and neck region. To find the gene expression signatures of ACC, we performed microarray experiments to compare ACC xenograft tumor models and normal tissue samples. We used microarrays to detail the global program of gene expression underlying adenoid cystic carcinoma and identified distinct classes of up- and down-regulated genes compared to non-neoplastic salivary tissue. Viable tumor tissue samples from human patients were used to establish xenograft tumor models in nude/nude immunodeficient mice. Tissue from these tumor models were compared to tissue samples of normal human salivary glands. Tissue samples were frozen, examined by cryostat histologic sectioning and macrodissected to obtain samples that represented at least 70% epithelial cells.
2012-03-26 | E-GEOD-36820 | biostudies-arrayexpress
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
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.
2013-10-01 | GSE25746 | GEO
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
Project description:tracheal adenoid cystic carcinoma is one kind of non-small-cell lung cancer with limit treatment options. We used single cell RNA sequencing (scRNA-seq) to analyze the molecular characteristic of tracheal adenoid cystic carcinoma, aiming to recognized this disease deeply and provide potential treatment plan in the future.
2024-10-31 | GSE245170 | GEO
Project description:Translocations that drive overexpression of the oncogenic transcription factor MYB are molecular hallmarks of adenoid cystic carcinoma (ACC), a malignant salivary gland tumor. Surgical resection, whenever possible, is the standard therapy for ACC, but there are no available therapeutic options available if surgery fails. Here we performed a chemical genetic screen using a zebrafish embryo culture system and identified retinoic acid agonists as potent suppressors of c-myb. Retinoic acid treatment strongly decreased c-myb gene expression in U937 cells and suggested a direct transcriptional mechanism of regulation. Retinoic acid agonists strongly inhibited tumor growth in vivo in different ACC patient derived xenograft models. Analysis of the xenografts revealed a significant decrease in MYB binding at translocated enhancers, thereby disrupting the MYB positive feedback loop that drives ACC. Our findings identify an important role of retinoic acid in MYB regulation and as a potential new effective therapy for ACC.
2018-08-11 | GSE98006 | GEO
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