Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Patterns of somatic uniparental disomy identify novel tumor suppressor genes in colorectal cancer

ABSTRACT: The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. This dataset includes the array CGH of 30 colorectal cancers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE64109 | GEO | 2015/09/02

SECONDARY ACCESSION(S): PRJNA270339

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Patterns of somatic uniparental disomy identify novel tumor suppressor genes in colorectal cancer

2015-09-02 | GSE64112 | GEO

Patterns of somatic uniparental disomy identify novel tumor suppressor genes in colorectal cancer

Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. This dataset includes the array CGH of 30 colorectal cancers.

2015-09-02 | GSE64110 | GEO

Patterns of somatic uniparental disomy identify driver tumor suppressor genes in colorectal cancer [Illumina]

Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. A total of 32 primary tumors from the colon and rectum were collected from the Hospital Clinic of Barcelona under the supervision of an experienced pathologist. DNA was extracted and bisulfited according to manufacturer's protocols. Matched patient DNA from normal mucosa was used as a reference for these experiments. This dataset includes methylation data for 29 colorectal cancers (only including those with good QC).

2015-09-02 | E-GEOD-64112 | biostudies-arrayexpress

Patterns of somatic uniparental disomy identify driver tumor suppressor genes in colorectal cancer [Agilent]

2015-09-02 | E-GEOD-64110 | biostudies-arrayexpress

Patterns of somatic uniparental disomy identify driver tumor suppressor genes in colorectal cancer [Affymetrix]

2015-09-02 | E-GEOD-64109 | biostudies-arrayexpress

Gene expression profiling of AML

Project description:AML/MDS patients carrying 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are characterized by a later onset, a complex aberrant karyotype (CAK) frequently including deletions within 5q, 17p and 7q, as well as fast progression of the disease with extremely poor prognosis. We and other have shown that the MLL gene is over expressed in amplified cases, however, in most of the cases the amplified region is not restricted to the MLL locus. In the present study we investigated 19 patients with AML/MDS and MLL gain/amplification [15 AML (two secondary, following MDS and PV, and three therapy related) and 4 MDS cases (two therapy related)]. By means of array CGH performed in 12 patients (GSE9928) we were able to delineate the minimal deleted regions within 5q, 17p and 7q and identified three independent regions 11q/I-III that were amplified in all cases. Gene expression profiles established in 15 cases were used to define the candidate genes within these regions. Interestingly, analysis of our data suggests an interdependency of genes influenced by losses of 5q and 17p and expression of genes present in 11q23-25. Additionally, we demonstrate that the gene expression signature can be used to discriminate AML/MDS with MLL amplification from all other types of AML, thus, indicating specific pathogenesis present in this entity. Keywords: AML patients, tumor stratification

2008-11-18 | GSE10258 | GEO

Transcription profiling of human acute myeloid leukemia patients

2008-11-22 | E-GEOD-10258 | biostudies-arrayexpress

Dynamics of genome alterations in Crohn’s disease associated colorectal carcinogenesis

Project description:To determine the pattern of copy number alterations that characterizes Crohn’s disease associated colorectal carcinomas (CD-CRCs), we performed array-based comparative genomic hybridization (aCGH) of CD-CRCs. As control group, we used histomorphologically similar sporadic mucinous colorectal adenocarcinomas. To gain insight into the dynamics of copy number alterations in CD associated colorectal tumor development, we additionally analyzed non-dysplastic, i.e., normal or inflamed, mucosa samples and dysplastic lesions from CD-CRC patients by aCGH. This revealed the gain of chromosome arm 5p as a distinctive feature of CD related colorectal carcinogenesis, while the overall pattern of copy number changes in CD-CRC was similar to sporadic mucinous CRC, including gains of chromosomes and chromosome arms 7, 8, 13 and 20q, and losses of 5q, 8p, 17p and 18q.

2018-06-30 | GSE113015 | GEO

Homo sapiens

Project description:Losses of chromosome 5q and 14q mark a subset of gastric cancers with good clinical outcome

| PRJNA136835 | ENA

Analysis of AML/MDS patients with 11q/MLL amplification

Project description:AML/MDS patients carrying 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are characterized by a complex aberrant karyotype (CAK) frequently including deletions within 5q, 17p and 7q, a later onset and fast progression of the disease with extremely poor prognosis. We and others have shown that the MLL gene is overexpressed in amplified cases; however, in most of the cases the amplified region is not restricted to the MLL locus. In the present study we investigated 19 patients with AML/MDS and MLL gain/amplification. By means of array CGH performed in 12 patients we were able to delineate the minimal deleted regions within 5q, 17p and 7q and identified three independent regions 11q/I-III that were amplified in all cases. Gene expression profiles established in 15 cases (GSE10258) were used to define candidate genes within these regions. Interestingly, analysis of our data suggests an interdependency of loss of 5q and 17p and expression of genes present in 11q23-25. Furthermore, we demonstrate that the gene expression signature can be used to discriminate AML/MDS with MLL amplification from several other types of AML, thus, indicating specific pathogenesis present in this entity. Keywords: comparative genomic hybridization; array CGH

2008-07-01 | GSE9928 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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