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Links from GEO DataSets

Items: 20

1.

A unifying gene signature for adenoid cystic cancer identifies parallel MYB-dependent and MYB-independent therapeutic targets

(Submitter supplied) MYB activation is proposed to underlie development of adenoid cystic cancer (ACC), an aggressive salivary gland tumor with no effective systemic treatments. To discover druggable targets for ACC, we performed global mRNA/miRNA analyses of 12 ACC with matched normal tissues, and compared these data with 14 mucoepidermoid carcinomas (MEC) and 11 salivary adenocarcinomas (ADC). We detected a unique ACC gene signature of 1160 mRNAs and 22 miRNAs. more...
Organism:
Homo sapiens; synthetic construct
Type:
Expression profiling by array; Non-coding RNA profiling by array
Platforms:
GPL6244 GPL8786
48 Samples
Download data: CEL
Series
Accession:
GSE59702
ID:
200059702
2.

A unifying gene signature for adenoid cystic cancer identifies parallel MYB-dependent and MYB-independent therapeutic targets (mRNA)

(Submitter supplied) MYB activation is proposed to underlie development of adenoid cystic cancer (ACC), an aggressive salivary gland tumor with no effective systemic treatments. To discover druggable targets for ACC, we performed global mRNA/miRNA analyses of 12 ACC with matched normal tissues, and compared these data with 14 mucoepidermoid carcinomas (MEC) and 11 salivary adenocarcinomas (ADC). We detected a unique ACC gene signature of 1160 mRNAs and 22 miRNAs. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
24 Samples
Download data: CEL
Series
Accession:
GSE59701
ID:
200059701
3.

A unifying gene signature for adenoid cystic cancer identifies parallel MYB-dependent and MYB-independent therapeutic targets (microRNA)

(Submitter supplied) MYB activation is proposed to underlie development of adenoid cystic cancer (ACC), an aggressive salivary gland tumor with no effective systemic treatments. To discover druggable targets for ACC, we performed global mRNA/miRNA analyses of 12 ACC with matched normal tissues, and compared these data with 14 mucoepidermoid carcinomas (MEC) and 11 salivary adenocarcinomas (ADC). We detected a unique ACC gene signature of 1160 mRNAs and 22 miRNAs. more...
Organism:
Homo sapiens; synthetic construct
Type:
Non-coding RNA profiling by array
Platform:
GPL8786
24 Samples
Download data: CEL
Series
Accession:
GSE59700
ID:
200059700
4.

Clinically significant copy number alterations and complex rearrangements of MYB and NFIB in adenoid cystic carcinoma of the head and neck

(Submitter supplied) Using high-resolution, array-based comparative genomic hybridization (aCGH), we explored genomic alterations in 40 fresh-frozen ACC samples, the largest cohort to date, with the aims to: (1) identify recurrent CNAs in ACC; (2) identify novel candidate target genes; and (3) correlate recurrent CNAs with tumour grade and other clinical parameters to identify potential clinically useful biomarkers.
Organism:
Homo sapiens
Type:
Genome variation profiling by genome tiling array
Platform:
GPL4091
40 Samples
Download data: TXT
Series
Accession:
GSE34816
ID:
200034816
5.

Expression data of 13 surgical samples of adenoid cystic carcinoma (ACC), 2 ACC xenografts, and 7 normal salivary gland tissues (NSGs)

(Submitter supplied) This experiment investigates differences in global gene expression between ACC and NSG.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
22 Samples
Download data: CEL, CHP
Series
Accession:
GSE88804
ID:
200088804
6.

Expression data after knockdown of MYB-NFIB and IGF1R/INSR inhibition in ACC cells

(Submitter supplied) The MYB-NFIB gene is a driver-mutation in the majority of adenoid cystic carcinomas (ACCs) and believed to control a large number of genes involved in tumorigenesis. This experiment investigates the effects on gene expression after siRNA knock-down of MYB-NFIB and/or inhibition of IGF1R/INSR signaling in ACC cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
18 Samples
Download data: CEL, CHP
Series
Accession:
GSE76094
ID:
200076094
7.

Xenograft model systems of adenoid cystic carcinoma

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3977
Platform:
GPL570
22 Samples
Download data: CEL
Series
Accession:
GSE28996
ID:
200028996
8.
Full record GDS3977

Adenoid cystic carcinoma xenograft models

Analysis of xenograft tumors derived from clinical samples of adenoid cystic carcinomas (ACC) implanted into immunodeficient nu/nu mice within 36 hrs of tissue being removed from the human subjects. Results provide insight into molecular mechanisms underlying the pathology of ACC.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 13 other, 2 tissue sets
Platform:
GPL570
Series:
GSE28996
22 Samples
Download data: CEL
9.

An oncogenic MYB feedback loop drives alternate cell fates in adenoid cystic carcinoma

(Submitter supplied) Translocation events are frequent in cancer and may create chimeric fusions or ‘regulatory rearrangements’ that drive oncogene overexpression. Here we identify super-enhancer translocations that drive overexpression of the oncogenic transcription factor MYB as a recurrent theme in adenoid cystic carcinoma (ACC). Whole-genome sequencing data and chromatin maps reveal distinct chromosomal rearrangements that juxtapose super-enhancers to the MYB locus. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL15520 GPL18573
46 Samples
Download data: BED, TDF
Series
Accession:
GSE76465
ID:
200076465
10.

Increased retinoic acid signalling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway [scRNA-seq]

(Submitter supplied) MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: MTX, TSV
Series
Accession:
GSE217084
ID:
200217084
11.

Increased retinoic acid signalling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway [RNA-seq_treated]

(Submitter supplied) MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28337
15 Samples
Download data: TXT
Series
Accession:
GSE217083
ID:
200217083
12.

Increased retinoic acid signalling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway [RNA-seq_KD]

(Submitter supplied) MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28337
18 Samples
Download data: TXT
Series
Accession:
GSE217082
ID:
200217082
13.

Increased retinoic acid signalling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway [ChIP-seq]

(Submitter supplied) MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
2 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE217081
ID:
200217081
14.

Increased retinoic acid signalling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway

(Submitter supplied) MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
10 Samples
Download data: XLS
Series
Accession:
GSE216913
ID:
200216913
15.

Increased retinoic acid signalling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL28337 GPL24676
41 Samples
Download data: BW, MTX, NARROWPEAK, TSV
Series
Accession:
GSE216852
ID:
200216852
16.

Expression profiling by high throughput sequencing of THP-1 cells treated with Monensin

(Submitter supplied) Purpose: to reveal gene expression changes induced by Monensin in THP-1 cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
Series
Accession:
GSE130657
ID:
200130657
17.

Retinoic acid suppresses MYB in adenoid cystic carcinoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: NARROWPEAK
Series
Accession:
GSE98008
ID:
200098008
18.

Retinoic acid suppresses MYB in adenoid cystic carcinoma [RNA-seq]

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: XLSX
19.

Retinoic acid suppresses MYB in adenoid cystic carcinoma [ChIP-seq]

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: NARROWPEAK
Series
Accession:
GSE98006
ID:
200098006
20.

Expression data of cultured MCF10A cells transduced with MYB or MYB-NFIB expression vectors

(Submitter supplied) This experiment investigates differences between control cells (empty vector) and cells with MYB or MYB-NFIB (M14N9) overexpression using MSCV vectors
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
9 Samples
Download data: CEL, CHP
Series
Accession:
GSE136095
ID:
200136095
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