Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Human glioma cells: chronophin (CIN/PDXP) knockdown vs. control or rescue

ABSTRACT: Transcriptional profiling of human glioma cells to elucidate the role of chronophin (CIN/PDXP) for glioma pathogenesis three-condition experiment: control cells vs. knockdown and knockdown vs. rescue

ORGANISM(S): Homo sapiens

SUBMITTER: Markus Schulze

PROVIDER: E-GEOD-71786 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Chronophin is a glial tumor modifier involved in the regulation of glioblastoma growth and invasiveness.

Schulze M M Fedorchenko O O Zink T G TG Knobbe-Thomsen C B CB Kraus S S Schwinn S S Beilhack A A Reifenberger G G Monoranu C M CM Sirén A-L AL Jeanclos E E Gohla A A

Oncogene 20151109 24

Glioblastoma is the most aggressive primary brain tumor in adults. Although the rapid recurrence of glioblastomas after treatment is a major clinical challenge, the relationships between tumor growth and intracerebral spread remain poorly understood. We have identified the cofilin phosphatase chronophin (gene name: pyridoxal phosphatase, PDXP) as a glial tumor modifier. Monoallelic PDXP loss was frequent in four independent human astrocytic tumor cohorts and increased with tumor grade. We found ...[more]

PMID: 26549022

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Project description:Samples were taken from colorectal cancers in surgically resected specimens in 33 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes that can be used for molecular markers for CIN phynotype Specimens from 33 consecutive stage II and stage III patients who had undergone surgical resection of CRC were studied. Patients with familial adenomatous polyposis and HNPCC were excluded from the study. Specimens from tumors and corresponding normal tissues in surgically resected specimens were snap-frozen in liquid nitrogen and stored at -80degreesC until use. Parallel tumor specimens were formalin fixed and paraffin embedded for histological examination. DNA and RNA was extracted from paired tumor and normal tissue using frozen samples. The patients provided written, informed consent to the collection of specimens, and the local Ethics Committee approved the study protocol. MSI and LOH phenotype analysis were done as follows; Using DNA, we performed the polymerase chain reaction (PCR) and determined the MSI status. In addition to five microsatellite markers recommended by the National Cancer Institute workshop, we also used TP53, D18S46, D18S363 and D18S474.9 We determined LOH status in non–MSI-high tumors, because LOH is rare in MSI-high tumors and also interpretation of LOH is difficult in MSI-high tumors. We defined LOH at each locus as a 50% reduction in the height of one of two allele peaks in tumor DNA relative to non-neoplastic control DNA. LOH was defined as present if any of the markers on the same chromosome show LOH. In order to evaluate the severity of chromosomal instability based on the actual frequency of LOH among evaluable loci, we defined the LOH Ratio (%) as: LOH Ratio (%) = Total number of chromosomes with LOH / Total number of chromosomes that could be evaluated for LOH × 100. Depending on the LOH Ratio, we classified tumors as having high levels of chromosomal instability (CIN-high) (33% < LOH Ratio < 100%) or low levels of chromosomal instability (CIN-low) (0% < LOH Ratio <33%). Furthermore, CIN-high tumors were divided into two subgroups; CIN-high (mild type) (33% < LOH Ratio < 75%) and CIN-high (severe type) (75% < LOH Ratio <100%).

Dataset Information

Human glioma cells: chronophin (CIN/PDXP) knockdown vs. control or rescue

Publications

Chronophin is a glial tumor modifier involved in the regulation of glioblastoma growth and invasiveness.

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