Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The DNA Double-Strand Break Response Is Abnormal in Myeloblasts From Patients With Therapy-Related Acute Myeloid Leukemia [Affymetrix]

ABSTRACT: In order to examine if the upregulation of DNA repair genes on chromosome 8 was associated with the abnormal DSB phenotype observed in trisomy 8 (defined by array CGH or cytogenetics), we compared the mRNA levels of DNA repair genes on chromosome 8 in trisomy 8 t-AML patients versus normal t-AML gammaH2AX responders using gene expression array data.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52478 | GEO | 2013/11/19

SECONDARY ACCESSION(S): PRJNA229072

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The DNA Double-Strand Break Response Is Abnormal in Myeloblasts From Patients With Therapy-Related Acute Myeloid Leukemia

Project description:In order to examine if the upregulation of DNA repair genes on chromosome 8 was associated with the abnormal DSB phenotype observed in trisomy 8 (defined by array CGH or cytogenetics), we compared the mRNA levels of DNA repair genes on chromosome 8 in trisomy 8 t-AML patients versus normal t-AML gammaH2AX responders using gene expression array data. Bone marrow cells taken directly from patients after written informed consent were cryopreserved, RNA extracted, and microarray analysis was performed using Affymetrix U133plus2 chips.

2013-11-19 | E-GEOD-52478 | biostudies-arrayexpress

The DNA Double-Strand Break Response Is Abnormal in Myeloblasts From Patients With Therapy-Related Acute Myeloid Leukemia [NimbleGen]

Project description:In order to examine if acquired copy number alterations in DNA repair genes is commonly observed in therapy-related AML, we used this custom built NimbleGen array with dense tiling of probes in 170 DNA repair genes to interrogate paired normal (skin) and tumor (bone marrow) samples.

2013-12-13 | GSE53250 | GEO

The DNA double-strand break response is abnormal in myeloblasts from patients with therapy-related acute myeloid leukemia.

Project description:The complex chromosomal aberrations found in therapy-related acute myeloid leukemia (t-AML) suggest that the DNA double-strand break (DSB) response may be altered. In this study we examined the DNA DSB response of primary bone marrow cells from t-AML patients and performed next-generation sequencing of 37 canonical homologous recombination (HR) and non-homologous end-joining (NHEJ) DNA repair genes, and a subset of DNA damage response genes using tumor and paired normal DNA obtained from t-AML patients. Our results suggest that the majority of t-AML patients (11 of 15) have tumor-cell intrinsic, functional dysregulation of their DSB response. Distinct patterns of abnormal DNA damage response in myeloblasts correlated with acquired genetic alterations in TP53 and the presence of inferred chromothripsis. Furthermore, the presence of trisomy 8 in tumor cells was associated with persistently elevated levels of DSBs. Although tumor-acquired point mutations or small indels in canonical HR and NHEJ genes do not appear to be a dominant means by which t-AML leukemogenesis occurs, our functional studies suggest that an abnormal response to DNA damage is a common finding in t-AML.

| S-EPMC4047198 | biostudies-literature

Monitoring Homology Search during DNA Double-Strand Break Repair in vivo

Project description:Homologous recombination (HR) is crucial for genetic exchange, accurate repair of DNA double-strand breaks and pivotal for genome integrity. HR uses homologous sequences for repair, but how homology search, the exploration of the genome for homologous DNA sequences, is conducted in the nucleus remains poorly understood. Here, we use time-resolved chromatin immunoprecipitations of repair proteins to monitor homology search in vivo. We found that homology search proceeds by a probing mechanism, which commences around the break and samples preferentially on the broken chromosome. However, elements thought to instruct chromosome loops mediate homology search shortcuts, and centromeres, which cluster within the nucleus, may facilitate homology search on other chromosomes. Our study thus revealed crucial parameters for homology search in vivo and emphasizes the importance of linear distance, chromosome architecture and proximity for recombination efficiency. 2 new custom ChIP-chip platforms used; both Nimblegen; differ in oligo density: (platform 1: 2006-07-18_Scerevisiae_ChIP_Stefan Jentsch MPI Biochemistry S.cerevisiae 385K Tiling Array Version 1) ( platform 2: 100304_Scer2_MS_Chip_Stefan Jentsch MPI Biochemistry S.cerevisiae 135K Tiling Array Version 2) ChIP-chip profiling of DSB repair factors (Rad51, Rad52, RPA, gamma-H2A) upon single inducible DSBs in S.cerevisiae

2013-03-21 | E-GEOD-44844 | biostudies-arrayexpress

caArray_krahe-00060: Expression profiling reveals fundamental biological differences in acute myeloid leukemia

Project description:Acute myeloid leukemia (AML) is a heterogeneous group of diseases. Normal cytogenetics (CN) constitutes the single largest group, while trisomy 8 (+8) as a sole abnormality is the most frequent trisomy. How trisomy contributes to tumorigenesis is unknown. We used oligonucleotide-based DNA microarrays to study global gene expression in AML+8 patients with +8 as the sole chromosomal abnormality and AML-CN patients. CD34+ cells purified from normal bone marrow (BM) were also analyzed as a representative heterogeneous population of stem and progenitor cells. Expression patterns of AML patients were clearly distinct from those of CD34+ cells of normal individuals. We show that AML+8 blasts overexpress genes on chromosome 8, estimated at 32% on average, suggesting gene-dosage effects underlying AML+8. Systematic analysis by cellular function indicated up-regulation of genes involved in cell adhesion in both groups of AML compared with CD34+ blasts from normal individuals. Perhaps most interestingly, apoptosis-regulating genes were significantly down-regulated in AML+8 compared with AML-CN. We conclude that the clinical and cytogenetic heterogeneity of AML is due to fundamental biological differences. **NOTE: Migrated from caArray 1.x, identifier='gov.nih.nci.ncicb.caarray:Experiment:1015897559579654:1' krahe-00060 Assay Type: Gene Expression Provider: Affymetrix Array Designs: Hu6800 Organism: Homo sapiens (ncbitax) Tissue Sites: Bone marrow Material Types: synthetic_DNA, synthetic_RNA, organism_part Cell Types: Myeloid Cell Disease States: Acute Myeloid Leukemia, Normal

2015-06-26 | E-GEOD-70284 | biostudies-arrayexpress

caArray_krahe-00060: Expression profiling reveals fundamental biological differences in acute myeloid leukemia

2015-06-26 | GSE70284 | GEO

The DNA Double-Strand Break Response Is Abnormal in Myeloblasts From Patients With Therapy-Related Acute Myeloid Leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-12-13 | GSE53251 | GEO

Monitoring Homology Search during DNA Double-Strand Break Repair in vivo

2013-03-21 | GSE44844 | GEO

Quantitative Genomic Analysis of RecA Protein Binding During DNA Double-Strand Break Repair Reveals RecBCD Action in vivo

Project description:Here we have developed a method that combines chromatin immunoprecipitation with next-generation sequencing (ChIP-Seq) and mathematical modeling to quantify RecA protein binding during the active repair of a single DSB in the chromosome of Escherichia coli. Examination of RecA binding during double-strand break repair in Escherichia coli

2015-08-11 | E-GEOD-71249 | biostudies-arrayexpress

RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [ChIP-seq]

Project description:In the bacterium Escherichia coli, RecBCD coordinates repair of two ends at a DNA double-strand break, preventing aberrant chromosome amplification

2018-07-18 | GSE107972 | GEO