Browse
Submit Data
Databases
API
Help

Dataset Information

15 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Genomic Complexity of Primary Human Prostate Cancer

ABSTRACT:

Seven primary prostate cancers and their paired normal counterparts were DNA-sequenced on a massively parallel sequencing platform. This approach was taken to investigate the genomes for mutations and genomic alterations that would be undetectable by lower-resolution methods. As result, tumors containing chains of balanced rearrangements that occurred within or adjacent to known cancer genes were discovered.

PROVIDER: phs000330.v1.p1 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Publications

The genomic complexity of primary human prostate cancer.

Berger Michael F MF Lawrence Michael S MS Demichelis Francesca F Drier Yotam Y Cibulskis Kristian K Sivachenko Andrey Y AY Sboner Andrea A Esgueva Raquel R Pflueger Dorothee D Sougnez Carrie C Onofrio Robert R Carter Scott L SL Park Kyung K Habegger Lukas L Ambrogio Lauren L Fennell Timothy T Parkin Melissa M Saksena Gordon G Voet Douglas D Ramos Alex H AH Pugh Trevor J TJ Wilkinson Jane J Fisher Sheila S Winckler Wendy W Mahan Scott S Ardlie Kristin K Baldwin Jennifer J Simons Jonathan W JW Kitabayashi Naoki N MacDonald Theresa Y TY Kantoff Philip W PW Chin Lynda L Gabriel Stacey B SB Gerstein Mark B MB Golub Todd R TR Meyerson Matthew M Tewari Ashutosh A Lander Eric S ES Getz Gad G Rubin Mark A MA Garraway Levi A LA

Nature 20110201 7333

Prostate cancer is the second most common cause of male cancer deaths in the United States. However, the full range of prostate cancer genomic alterations is incompletely characterized. Here we present the complete sequence of seven primary human prostate cancers and their paired normal counterparts. Several tumours contained complex chains of balanced (that is, 'copy-neutral') rearrangements that occurred within or adjacent to known cancer genes. Rearrangement breakpoints were enriched near ope ...[more]

PMID: 21307934

Similar Datasets

The Genomic Complexity of Primary Human Prostate Cancer

Project description:<p>Seven primary prostate cancers and their paired normal counterparts were DNA-sequenced on a massively parallel sequencing platform. This approach was taken to investigate the genomes for mutations and genomic alterations that would be undetectable by lower-resolution methods. As result, tumors containing chains of balanced rearrangements that occurred within or adjacent to known cancer genes were discovered.</p>

| phs000330 | dbGaP

Genome-wide analysis of the binding pattern of the transcriptional co-activator Cbp.

Project description:The transcriptional coactivator Cbp is critical for hematopoietic stem cell (HSC) development. However, its role in adult HSC and the mechanistic detail of Cbp control of HSC function remain unknown. Using conditional deletion of Cbp in the adult HSC compartment, we demonstrate an altered balance between differentiation and self-renewal with gradual loss of phenotypic HSC, differentiation defects in lower compartments and the development of myeloid malignancies. In addition, we demonstrate that Cbp -/- HSCs reconstitute hematopoiesis with lower efficiency than their wild type counterparts and readily exhaust over time when placed under the replicative stress of serial transplantation. Furthermore, we demonstrate abnormal cell cycle (re)entry and apoptosis in HSC which, with preferential differentiation, also contribute to stem cell exhaustion. Finally we demonstrate global transcriptional abnormalities predicted to alter cell cycle control, balanced differentiation and HSC function upon Cbp deletion and link Cbp to a critical HSC transcriptional regulatory network through genome-wide analysis of Cbp binding. 1 sample (Cbp) and 1 control, all prepared from a hematopoietic progenitor/stem cell line (BM-HPC)

2011-12-15 | E-GEOD-25265 | biostudies-arrayexpress

Genome-wide analysis of the binding pattern of the transcriptional co-activator Cbp.

2011-12-15 | GSE25265 | GEO

NanoString miRNA profiling of peripheral blood mononuclear cells from HIV-1-infected elite suppressors, viremic patients, and uninfected control donors

Project description:This study used the NanoString nCounter hybridization system and nCounter miRNA expression assays to identify and quantitate circulating cellular miRNAs during HIV-1 elite suppression, active HIV-1 replication, and uninfected status. Blood samples were from eight uninfected controls, seven HIV-1 elite suppressors with undetectable viral load, and six viremic HIV-1-infected patients.

2012-02-22 | E-GEOD-33387 | biostudies-arrayexpress

Gene expression analysis of Cbp deficient LSK cells

Project description:The transcriptional coactivator Cbp is critical for hematopoietic stem cell (HSC) development. However, its role in adult HSC and the mechanistic detail of Cbp control of HSC function remains unknown. Using conditional deletion of Cbp in the adult HSC compartment, we demonstrate an altered balance between differentiation and self-renewal with gradual loss of phenotypic HSC, differentiation defects in lower compartments and the development of myeloid malignancies. In addition, we demonstrate that Cbp -/- HSCs reconstitute hematopoiesis with lower efficiency than their wild type counterparts and readily exhaust over time when placed under the replicative stress of serial transplantation. Furthermore, we demonstrate abnormal cell cycle (re)entry and apoptosis in HSC which, with preferential differentiation, also contribute to stem cell exhaustion. Finally we demonstrate global transcriptional abnormalities predicted to alter cell cycle control, balanced differentiation and HSC function upon Cbp deletion and link Cbp to a critical HSC transcriptional regulatory network through genome-wide analysis of Cbp binding. Genome-wide gene expression analysis of LSK population after Cbp deletion. The LSK population of bone marrow is enriched for hematopoietic stem cells. Total RNA was extracted from flow-sorted LSK population of bone marrow, 4 weeks after pIpC induced deletion of Cbp. 2 replicates for Cbp wt control, 2 replicates for Cbp Mx.

2011-12-15 | E-GEOD-25268 | biostudies-arrayexpress

Gene expression analysis of Cbp deficient LSK cells

Project description:The transcriptional coactivator Cbp is critical for hematopoietic stem cell (HSC) development. However, its role in adult HSC and the mechanistic detail of Cbp control of HSC function remains unknown. Using conditional deletion of Cbp in the adult HSC compartment, we demonstrate an altered balance between differentiation and self-renewal with gradual loss of phenotypic HSC, differentiation defects in lower compartments and the development of myeloid malignancies. In addition, we demonstrate that Cbp -/- HSCs reconstitute hematopoiesis with lower efficiency than their wild type counterparts and readily exhaust over time when placed under the replicative stress of serial transplantation. Furthermore, we demonstrate abnormal cell cycle (re)entry and apoptosis in HSC which, with preferential differentiation, also contribute to stem cell exhaustion. Finally we demonstrate global transcriptional abnormalities predicted to alter cell cycle control, balanced differentiation and HSC function upon Cbp deletion and link Cbp to a critical HSC transcriptional regulatory network through genome-wide analysis of Cbp binding. Genome-wide gene expression analysis of LSK population after Cbp deletion. The LSK population of bone marrow is enriched for hematopoietic stem cells.

2011-12-15 | GSE25268 | GEO

Seven chain adaptive immune receptor repertoire analysis in rheumatoid arthritis reveals novel features associated with disease and clinically relevant phenotypes

Project description:In rheumatoid arthritis (RA), the activation of T and B cell clones specific for self-antigens leads to the chronic inflammation of the synovium. Here, we perform an in-depth quantitative analysis of the seven chains that comprise the adaptive immune receptor repertoire (AIRR) in RA. In comparison to controls, we show that RA patients have multiple and strong differences in the BCR repertoire including reduced diversity as well as altered isotype, chain and segment frequencies. We demonstrate that therapeutic TNF inhibition partially restores this alteration but find a profound difference in the underlying biochemical reactivities between responders and non-responders. Combining the AIRR with HLA typing, we identify the specific TCR repertoire associated with disease risk variants. Integrating these features, we further develop a molecular classifier that shows the utility of the AIRR as a diagnostic tool. Simultaneous sequencing of the seven chains of the human AIRR reveals novel features associated with the disease and clinically relevant phenotypes, including response to therapy. These findings show the unique potential of AIRR to address precision medicine in immune-related diseases.

2024-02-23 | GSE256256 | GEO

Systematic dissection of regulatory motifs in 2,000 predicted human enhancers using a massively parallel reporter assay

Project description:We employ a massively parallel reporter assay (MPRA) to measure the ex vivo activities of hundreds of K562 and HepG2 enhancers with known transcription factor motif instances. For seven selected motifs that correspond to known or predicted activators and repressors in the two cell types, we make directed modifications of the bases corresponding to these motifs and observe the changes in enhancer activity.

2013-03-15 | GSE33367 | GEO

Genome-wide comparison of trisomy 21 iPSCs and derived isogenic disomy 21 iPSCs.

Project description:Human trisomies can alter cellular phenotypes and produce congenital abnormalities such as Down Syndrome (DS). Here we have generated induced pluripotent stem cells (iPSCs) from DS fibroblasts, and introduced a TKNEO transgene into one copy of chromosome 21 by gene targeting. When selecting against TKNEO, spontaneous chromosome loss was the most common cause for survival, with a frequency of ~10-4, while point mutations, epigenetic silencing, and TKNEO deletions occurred at lower frequencies in this unbiased comparison of inactivating mutations. Mitotic recombination events resulting in extended loss of heterozygosity were not observed in DS iPSCs. The disomic cells that we derived proliferated faster and produced more endothelia in vivo than their otherwise isogenic trisomic counterparts, but hematopoietic differentiation, pluripotency and survival were statistically unchanged. Our study describes the first targeted removal of a human trisomy, which could prove useful in both clinical and research applications. RNA samples were from two trisomic iPSC clone (C2-4, C3-5) and four derived disomic subclones (C2-4-3, C2-4-4 and C3-5-11, C3-5-13). Duplicate RNA samples from human embyonic stem cells (H1) were included as control.

2012-10-23 | E-GEOD-38931 | biostudies-arrayexpress

Development of distinct gene expression signature in neurons from different regions of the brain

Project description:We have performed microarray expression profiling of mouse primary neurons (cortical neurons and granule cell neurons) to model molecular networks and define whether distinct antiviral IFN responses occurred in neurons corresponding to different brain regions. Primary mouse cortical neurons and granule cell neurons were left untreated, treated with 100IU/mL of IFN-M-NM-2, or infected with West Nile virus (MOI of 1) and RNA was harvested after 24 hours. Three independent experiments were performed using a balanced design.

2012-12-05 | E-GEOD-42727 | 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