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Expression data from AID-silenced mouse plasmacytoma J558 (BALB/c, H-2Ld)cell lines

ABSTRACT: To determine the potential mechanisms by which AID-elimination facilitate better J558 tumor rejection by P1CTL, we performed cDNA microarray analysis to compare AID-silenced J558 cells and their relative controls.

ORGANISM(S): Mus musculus

PROVIDER: GSE19110 | GEO | 2009/11/20

SECONDARY ACCESSION(S): PRJNA120463

REPOSITORIES: GEO

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Transcription profiling of mous eAID-silenced plasmacytoma J558 (BALB/c, H-2Ld)cell lines

Project description:To determine the potential mechanisms by which AID-elimination facilitate better J558 tumor rejection by P1CTL, we performed cDNA microarray analysis to compare AID-silenced J558 cells and their relative controls. Experiment Overall Design: The mouse Affymetrix Mouse Genechips 430-2.0 arrays were hybridized to RNA derived from control and AID-silenced J558 cells according to manufacturerâs directions. Two different pairs of cells (C4 vs AID 2.27 (a) and C5 vs AID 2.13 (b)) were used for RNA extraction and hybridization on Affymetrix microarrays.

2009-12-02 | E-GEOD-19110 | biostudies-arrayexpress

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Project description:Activation-Induced Cytidine Deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center B lymphocytes. Occasionally, AID targets non-Ig genes, thereby contributing to B cell lymphomagenesis. We recently reported aberrant expression of AID in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). To elucidate the biological significance of aberrant AID expression, we studied loss of AID function in a murine model of BCR-ABL1 ALL. Mice transplanted with BCR-ABL1-transduced AID-/- bone marrow had prolonged survival as compared to mice transplanted with leukemia cells generated from AID+/+ bone marrow. Consistent with a causative role of AID in genetic instability, AID-/- leukemia had a decreased frequency of amplifications, deletions and a lower frequency of mutations in non-Ig genes including Pax5 and Rhoh as compared to AID+/+ leukemias. AID-/- and AID+/+ ALL cells showed a markedly distinct gene expression pattern as determined by principle component analysis, with 2,365 genes differentially expressed. In contrast to AID+/+ leukemia, AID-/- ALL cells failed to downregulate a number of tumor suppressor genes such as Rhoh, Cdkn1a (p21), and Blnk (SLP65). We conclude that AID accelerates clonal evolution in BCR-ABL1 ALL by enhancing genetic instability, aberrant somatic hypermutation, and by transcriptional inactivation of tumor suppressor genes. Experiment Overall Design: We used microarrays to detect differences in gene expression profiles between AID expressing leukemia and AID deficient leukemia

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CGH data from AID WT vs AID KO BCR-ABL1 mouse leukemia cells

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