Unknown,Transcriptomics,Genomics,Proteomics

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DLBCL Patients

ABSTRACT: Genomic profiles of DLBCL (Diffuse Large B-cell Lymphoma) patients 20 DLBCL patients were selected for detection of genomic aberrations Patient's DNA were hybridized against Promega control on Agilent G4410B arrays and scanned with the Agilent G2505B scanner.

ORGANISM(S): Homo sapiens

SUBMITTER: frederic lepretre

PROVIDER: E-GEOD-19459 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Waved aCGH: to smooth or not to smooth.

Leprêtre F F Villenet C C Quief S S Nibourel O O Jacquemin C C Troussard X X Jardin F F Gibson F F Kerckaert J P JP Roumier C C Figeac M M

Nucleic acids research 20100113 7

Array-based comparative genomic hybridization (aCGH) is a powerful tool to detect genomic imbalances in the human genome. The analysis of aCGH data sets has revealed the existence of a widespread technical artifact termed as 'waves', characterized by an undulating data profile along the chromosome. Here, we describe the development of a novel noise-reduction algorithm, waves aCGH correction algorithm (WACA), based on GC content and fragment size correction. WACA efficiently removes the wave arti ...[more]

PMID: 20071741

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Project description:Silencing of genes that suppress the malignant phenotype by DNA methylation spurred an interest in the clinical use of epigenetic reprogramming agents. Single therapy is unlikely to be curative in the context of a heterogeneous disease such as Diffuse Large B cell Lymphomas (DLBCL). The combination of DNA demethylating drugs could increase the chance to respond to classical and new treatments. We found that DLBCL cell lines respond heterogeneously to DNA demethylating agents. In sensitive cell lines, 5-aza-2’-deoxycytidine induced a genomic signature similar to that of doxorubicin, the most important drug of the combinatorial chemotherapy regimen for DLBCL treatment. Accordingly, the combination of 5-aza-2’-deoxycytidine and doxorubicin proved to be synergistic in cell killing in vitro and in vivo for DLBCL cell lines individually responsive to these drugs. In doxorubicin resistant cell lines, long-term exposure to low-dose of 5-aza-2’-deoxycytidine induces DNA demethylation and subsequent doxorubicin sensitization in vitro and in vivo. This later effect correlates with SMAD1 demethylation. SMAD1 is epigenetically silenced in doxorubicin-resistant DLBCL cells and DLBCL patients with poor prognostic. In addition, we found that DNA demethylating agents can sensitize primary DLBCL cells to doxorubicin. Primary cells obtained from a DLBCL patient treated with 5-azacytidine shows SMAD1 demethylation and ex vivo sensitization to multiple drugs. Therefore, DNA demethylating drugs can reprogram otherwise resistant DLBCL cells to respond to chemotherapy agents without increasing the toxicity to normal tissues. Our data also indicate that DNA methylation and consequent suppression of SMAD1 expression represent a previously undescribed molecular mechanism of chemoresistance in DLBCL that can be further exploit for therapy. A microarray study using genomic DNA from different DLBCL cell lines before any treatment. Two to four biological replicates by cell line. The HELP data wil be used to find genes hypermethylated in resistant cell lines compared to sensitive cell lines to doxorubicin and other drugs.

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DLBCL Patients

Publications

Waved aCGH: to smooth or not to smooth.

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