Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Copy number analysis of Hodgkin lymphoma cell lines KM-H2 and L-428

ABSTRACT: We identified copy number changes associated with fusion transcripts and breakpoints on chromosomes 15 and 16.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25989 | GEO | 2010/12/11

SECONDARY ACCESSION(S): PRJNA142355

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Copy number analysis of Hodgkin lymphoma cell lines KM-H2 and L-428

Project description:We identified copy number changes associated with fusion transcripts and breakpoints on chromosomes 15 and 16. Data integration with RNAseq data

2010-12-11 | E-GEOD-25989 | biostudies-arrayexpress

Melittin Increases Cisplatin Sensitivity and Kills KM-H2 and L-428 Hodgkin Lymphoma Cells.

Project description:Hodgkin lymphoma (HL) is neoplasia with high cure rates. However, not all patients can be cured with the current treatment. Chemo-resistance of tumor cells is one factor involved in treatment failure. In addition to its pore-forming activity on lipid bilayer membranes, the toxin melittin from bee venom is an inhibitor of several cancer-related signaling pathways. Moreover, melittin analogs have been shown to inhibit the activity of ATP binding cassette (ABC) transporters which are known to play important roles in the chemo-resistance of tumor cells. Therefore, we tested the toxicity of melittin for HL cell lines KM-H2 and L-428 and whether melittin can increase the chemo-sensitivity of cisplatin-resistant HL cells. We found high toxicity of melittin for KM-H2 and L-428 cells. In co-cultures with normal blood cells, melittin preferentially killed KM-H2 and L-428 cells. In addition, we observed increased cisplatin sensitivity of chemo-resistant L-428 cells after treatment with melittin. ABC transporter activity was not reduced after treatment with melittin. Our data suggest that melittin or melittin analogs might be promising agents for the future development of treatment strategies for HL patients with resistant disease.

| S-EPMC7795649 | biostudies-literature

Expression data from EBER1-overexpressing Hodgkin lymphoma cell lines KM-H2 and L428

Project description:Epstein-Barr virus (EBV)- encoded RNAs (EBERs) are aboundance in all EBV lantency, it was found that EBERs may contribute to the oncogenesis. To study the role of EBV-encoded small RNAs (EBERs) in Hodgkin lymphoma, we transfected Hodgkin lymphoma cell lines, KMH2 and L428, with EBER1 and screen with microarrays to verify what is the possible role of the EBER1 in Hodgkin lymphoma.

2010-02-13 | GSE12427 | GEO

Genomic copy number alterations in human esophageal squamous cell carcinoma (ESCC) cell lines

Project description:Characterization of copy number alterations and unbalanced breakpoints in human esophageal squamous cell carcinoma cell lines by array-based comparative genomic hybridization.

2013-02-28 | GSE36115 | GEO

Normalization of whole-genome SNP data from non-Hodgkin lymphoma patients for copy number variation.

Project description:With the whole genome SNPs array information, we could evaluate the copy number variation of samples so as to find out specific DNA aberrations in non-Hodgkin lymphma comparing with reactive hyperplasia patients.

2016-05-24 | GSE47357 | GEO

Copy number variation analysis on a non-Hodgkin lymphoma case-control study identifies an 11q25 duplication associated with diffuse large B-cell lymphoma

Project description:Recent GWAS have identified several susceptibility loci for NHL. Despite these successes, much of the heritable variation in NHL risk remains to be explained. Common copy-number variants are important genomic sources of variability, and hence a potential source to explain part of this missing heritability. In this study, we carried out a CNV analysis using GWAS data from 681 NHL cases and 749 controls to explore the relationship between common structural variation and lymphoma susceptibility. Here we found a novel association with diffuse large B-cell lymphoma (DLBCL) risk involving a partial duplication of the C-terminus region of the LOC283177 long non-coding RNA that was further validated by quantitative PCR. For chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), known somatic deletions were identified on chromosomes 13q14, 11q22-23, 14q32 and 22q11.22. Our study shows that GWAS data can be used to identify germline CNVs associated with disease risk for DLBCL and somatic CNVs for CLL/SLL.

2014-09-23 | GSE58718 | GEO

Copy number profiling of gastric cancer cell lines and gastric tumor tissues

Project description:Copy number profiling of 27 gastric cancer cell lines and 105 gastric tumor tissues. we hypothesized that a detailed fine-scale survey of genomic CNAs might reveal potential genes disrupted by fusion events in gastric cancer. We inferred the locations of likely chromosomal breakpoints by identifying regions where closely-spaced microarray probes exhibited striking transitions in copy number.

2010-12-31 | GSE22694 | GEO

DNA copy-number changes

Project description:Gene amplifications and deletions frequently contribute to tumorigenesis. Characterization of these DNA copy-number changes is important for both the basic understanding of cancer and its diagnosis. Comparative genomic hybridization (CGH) was developed to survey DNA copy-number variations across a whole genome. With CGH, differentially labelled test and reference genomic DNAs are co-hybridized to normal metaphase chromosomes, and fluorescence ratios along the length of chromosomes provide a cytogenetic representation of DNA copy-number variation. CGH, however, has a limited ( approximately 20 Mb) mapping resolution, and higher-resolution techniques, such as fluorescence in situ hybridization (FISH), are prohibitively labour-intensive on a genomic scale. Array-based CGH, in which fluorescence ratios at arrayed DNA elements provide a locus-by-locus measure of DNA copy-number variation, represents another means of achieving increased mapping resolution. Published array CGH methods have relied on large genomic clone (for example BAC) array targets and have covered only a small fraction of the human genome. cDNAs representing over 30,000 radiation-hybrid (RH)-mapped human genes provide an alternative and readily available genomic resource for mapping DNA copy-number changes. Although cDNA microarrays have been used extensively to characterize variation in human gene expression, human genomic DNA is a far more complex mixture than the mRNA representation of human cells. Therefore, analysis of DNA copy-number variation using cDNA microarrays would require a sensitivity of detection an order of magnitude greater than has been routinely reported. We describe here a cDNA microarray-based CGH method, and its application to DNA copy-number variation analysis in breast cancer cell lines and tumours. This study is described more fully in Pollack JR et al.(1999) Nat Genet 23:41-6 Keywords: other

2002-06-27 | GSE49 | GEO

A prospective study of mitochondrial DNA copy number and risk of non-Hodgkin lymphoma.

Project description:Mitochondrial DNA (mtDNA) copy number is increased in patients with chronic lymphocytic leukemia (CLL), in Burkitt lymphoma and Epstein-Barr virus-transformed lymphoblastoid cell lines, and in T cells activated via the T-cell receptor. We hypothesized that having a higher mtDNA copy number in peripheral white blood cell DNA from healthy subjects would be associated with future risk of non-Hodgkin lymphoma (NHL). We analyzed mtDNA copy number in 104 incident male NHL cases and 104 matched controls within the prospective Alpha-Tocopherol, Beta-Carotene (ATBC) Cancer Prevention cohort. There was a dose-response relationship between tertiles of mtDNA copy number and risk of NHL (odds ratio [OR], 95% confidence interval [CI]: 1.0; 1.4 [0.7-2.8]; and 2.4 [1.0-5.5], respectively; P(trend) = .046). The effect was most pronounced for the CLL/small lymphocytic lymphoma (SLL) subtype (OR: 1.0; 3.2 [0.7-15.7]; 14.1 [1.9-103.2]; P(trend) = .009). These results suggest that mtDNA copy number could be associated with the risk of NHL, particularly CLL/SLL.

| S-EPMC2582005 | biostudies-literature

Genomic copy number alterations in human esophageal squamous cell carcinoma (ESCC) cell lines

Project description:Characterization of copy number alterations and unbalanced breakpoints in human esophageal squamous cell carcinoma cell lines by array-based comparative genomic hybridization. Six cell lines

2013-02-28 | E-GEOD-36115 | biostudies-arrayexpress

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