Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomewide copy number profiles for Adenosarcoma patients in Taiwan

ABSTRACT: Müllerian adenosarcomas are malignant gynecologic neoplasms. Advanced disease stage and sarcomatous overgrowth predict aggressive clinical courses. We conducted this study to characterize the genomewide copy number variations (CNV) in adenosarcomas. Paraffin samples from 13 cases were subjected to CNV analysis using OncoScan® FFPE Assay Kit. CNVs were significantly higher in cases with sarcomatous overgrowth. Frequent amplifications of chromosomal segments in 12p12.3 and 12q13.3-23.3 were noted, involving established or potential oncogenes including PIK3C2G (5 cases), MDM2, CPM, YEATS4, CDK4, GLI1, DDIT3 (co-amplified in 4 cases), as well as HMGA2 in 3 cases. MDM2 and CDK4 amplification was verified by fluorescence in situ hybridization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67107 | GEO | 2016/12/31

SECONDARY ACCESSION(S): PRJNA278968

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Affymetrix OncoScan SNP arrays for profiling somatic copy-number alterations in blastic plasmacytoid dendritic cell neoplasm

Project description:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an aggressive malignancy assumed to originate from plasmacytoid dendritic cells (pDCs), which affects the skin and bone marrow and sequentially other organ systems. Here, we used Affymetrix OncoScan CNV arrays to characterize somatic copy number variations in 45 BPDCN cases.

2022-04-05 | GSE200113 | GEO

CDK4 inhibition diminishes p53 activation by Mdm2-antagonists

Project description:CDK4 inhibitors have reached clinical approval for cancer therapy. In parallel, the p53 antagonist Mdm2 remains an attractive target for anti-cancer therapy, including numerous clinical studies. The genes encoding Mdm2 and CDK4 are frequently co-amplified in human malignancies, most notably in liposarcomas, suggesting their combined targeting for therapy. Here we show, however, that small compounds that inhibit Mdm2 and CDK4 antagonize each other rather than synergize in their cytotoxicity towards sarcoma cells. CDK4 inhibition attenuates the induction of p53-responsive genes upon Mdm2 inhibition, and similar results were obtained when depleting Mdm2 and/or CDK4 with siRNA. CDK4 inhibitors also interfered with p53 activity in response to DNA damage. CDK4 inhibition did not reduce p53 binding or histone acetylation to promoters, but rather attenuated the subsequent recruitment of RNA polymerase II. The complexes of p53 and Mdm2, as well as CDK4 and Cyclin D1, physically associated with each other. Upon combined inhibition of Mdm2 and CDK4/6, the interaction of this complex was impaired. Thus, the CDK4-Cyclin D1 complex plays a key role in enabling the transcription of p53 target genes. Taken together, our results raise caution regarding the combination of CDK4 inhibitors with Mdm2 antagonists or conventional DNA-damaging chemotherapeutics in the clinics. Moreover, they suggest a hitherto unknown role for CDK4-cyclin D1 complex in sustaining p53 activity, possibly focusing p53-mediated transcription on actively proliferating cells.

2018-09-20 | GSE113369 | GEO

CDK4/6 inhibitor-mediated cell overgrowth triggers an osmotic stress response

Project description:Cell size and the cell cycle are intrinsically coupled and abnormal increases in cell size are associated with senescence and permanent cell cycle arrest. The mechanism by which overgrowth primes cells to withdraw from the cell cycle remains unknown. We investigate this here using CDK4/6 inhibitors that arrest cell cycle progression during G0/G1 and are used in the clinic to treat ER+/HER2- metastatic breast cancer. We demonstrate that CDK4/6 inhibition promotes cellular overgrowth during G0/G1, causing p38MAPK-p53-p21-dependent cell cycle withdrawal. We find that cell cycle withdrawal is triggered by two waves of p21 induction. First, overgrowth during a long-term G0/G1 arrest induces an osmotic stress response. This stress response produces the first wave of p21 induction. Second, when CDK4/6 inhibitors are removed, a fraction of cells escape long term G0/G1 arrest and enter S-phase where overgrowth-driven replication stress results in a second wave of p21 induction that causes cell cycle withdrawal from G2, or the subsequent G1. We propose a model whereby both waves of p21 induction contribute to promote permanent cell cycle arrest. This model could explain why cellular hypertrophy is associated with senescence and why CDK4/6 inhibitors have long-lasting effects in patients.

2023-11-27 | PXD036519 | Pride

OncoScan analysis of breast carcinomas from the Swedish haemangioma cohort

Project description:The Swedish haemangioma cohort consists of 17,200 women treated with radium-226 for skin haemangioma at an early age (<1.5 years of age) between 1920 and 1965. A total of 877 breast cancer cases were reported by December 2009, estimating an excess relative and absolute risk at the age of 50 years of 0.48 Gy^(−1) and 10.4 (10^4 PYR Gy)^(−1), respectively. We screened 31 primary breast carcinomas for genetic alterations using the OncoScan CNV Plus Assay to assess genomic instability.

2019-04-12 | GSE125700 | GEO

Affymetrix OncoScan FFPE Microarray data for Malignant Pleural Mesothelioma Samples

Project description:For establishing a live-cell biobank of Malignant Pleural Mesothelioma (MPM) samples, cultures of two MPM patients were compared to the original tumor tissue using Affymetrix OncoScan Microarrays for genome-wide CNV and LOH detection.

2018-01-18 | GSE109305 | GEO

OncoScan CNV array data for PNBX cohort

Project description:OncoScan CNV array data for PNBX cohort

| PRJNA613943 | ENA

Oncogenic signals prime cancer cells for toxic cell growth during a G1 cell cycle arrest

Project description:A long-term goal in cancer research has been to inhibit the cell cycle in tumour cells without causing toxicity in proliferative healthy tissues. The best evidence that this is achievable is provided by CDK4/6 inhibitors, which arrest the cell cycle in G1, are well-tolerated in patients, and are effective in treating ER+/HER2- breast cancer. CDK4/6 inhibitors are effective because they arrest tumour cells more efficiently than some healthy cell types and, in addition, they affect the tumour microenvironment to enhance anti-tumour immunity. We demonstrate here another reason to explain their efficacy. Tumour cells are specifically vulnerable to CDK4/6 inhibition because during the G1 arrest, oncogenic signals drive toxic cell overgrowth. This overgrowth causes permanent cell cycle withdrawal by either preventing progression from G1 or by inducing replication stress and genotoxic damage during the subsequent S-phase and mitosis. Inhibiting or reverting oncogenic signals that converge onto mTOR can rescue this excessive growth, DNA damage and cell cycle exit in cancer cells. Conversely, inducing oncogenic signals in non-transformed cells can drive these toxic phenotypes and sensitize cells to CDK4/6 inhibition. Together, this demonstrates how oncogenic signals that have evolved to stimulate constitutive tumour growth and proliferation driven subverted to cause toxic cell growth and irreversible cell cycle exit when proliferation is halted in G1.

2023-11-17 | PXD043792 | Pride

OncoScan CNV SNP array data for MNG/PTC samples

Project description:OncoScan CNV SNP array data for MNG/PTC samples

| PRJNA558681 | ENA

Oncoscan SNP arrays for study "Molecular and functional profiling of plasmablastic lymphoma"

Project description:1 cell line and 82 Oncoscan SNP tumor initial samples, zipped Affymetrix CEL file types, Oncoscan CNV FFPE Assay Kit, Thermo Fisher Scientific GeneChipTM Scanner 3000 7G

| EGAD00010001978 | EGA

Integrated Copy Number Analysis of Epstein Barr Virus (EBV)-Positive Diffuse Large B-Cell Lymphoma (DLBCL)

Project description:Copy number analysis was performed on EBV+ DLBCL samples compared with EBV- DLBCL. We analyzed the genomic DNA from 18 cases of EBV+ DLBCL, 21 cases of EBV- DLBCL, and 13 cases of nonneoplastic tonsillar tissues using OncoScan FFPE Express 2.0 (MIP). No technical replication were done.

2014-02-01 | E-MTAB-1971 | 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