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Organ-specific Profiles of Genetic Alterations in Liver, Stomach and Lung Cancers caused by AID Expression

ABSTRACT: To analyze the organ-specific genetic changes in the tumor-related genes commonly triggerd by the AID-mediated mutagenesis, we compared the gene expression profiles among epitherial tumors developed in AID Tg mouse. Keywords: genetic alteration

ORGANISM(S): Mus musculus

PROVIDER: GSE9304 | GEO | 2007/10/27

SECONDARY ACCESSION(S): PRJNA102953

REPOSITORIES: GEO

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Transcription profiling of mouse liver, stomach and lung cancers caused by AID expression in the AID Tg mouse

Project description:To analyze the organ-specific genetic changes in the tumor-related genes commonly triggerd by the AID-mediated mutagenesis, we compared the gene expression profiles among epitherial tumors developed in AID Tg mouse. Experiment Overall Design: We analyzed the up or down regulated genes in tumor tissues compared with nontumor tissues in AID Tg mouse (see Supplementary table at the foot of the record). We compared each gene expression profile among three epitherial tumors in AID Tg mouse.

2008-06-16 | E-GEOD-9304 | biostudies-arrayexpress

Expression profiles of liver tissues from wild-type and AID transgenic mice exposed to thioacetamide hepatotoxicity

Project description:AID is an intrinsic DNA mutator enzyme and contributes to tumorigenesis through the accumulation of genetic aberrations. To examine whether mutagenesis induced by AID during inflammation-associated hepatocarcinogenesis depends on the transcriptional levels of the target genes, we performed the gene expression profiling of liver tissues from AID transgenic mice and wild-type mice with and without thioacetamide treatment. AID transgenic mice and wild-type mice were administered with thioacetamide in drinking water for 6 months, and the gene expression levels of their livers are compared.

2015-07-10 | E-GEOD-62878 | biostudies-arrayexpress

Expression profiles of liver tissues from wild-type and AID transgenic mice exposed to thioacetamide hepatotoxicity

2015-07-10 | GSE62878 | GEO

Transcription profiling of AID expressing leukemia and AID deficient leukemia in a mouse model of BCR-ABL1 ALL

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

2009-07-05 | E-GEOD-16751 | biostudies-arrayexpress

AID BioID data for Methot et al, "A licensing step links AID to transcriptional elongation for mutagenesis in B cells", Nat. Commun. 2018

Project description:These files represent the raw spectrum files obtained from the AID BioID experiments described in "A licensing step links AID to transcriptional elongation for mutagenesis in B cells", Nat. Commun. 2018. Detailed description of the BioID experiment protocol is available in the article. Briefly, APOBEC2, AID, AID-R171Y or AID-R178D were C-terminally tagged with BirA* and the constructs were expressed in AID-/- mouse primary B cells ex vivo. These cells were activated with LPS+IL4. After 24hrs, the cells were supplemented with biotin. 24hr later cells were harvested and biotinylated proteins were captured with Streptavidin sepharose beads, followed by on-bead trypsinization. Trypsinized peptides were identified by LC-MS/MS using Thermo Orbitrap Fusion, employing HCD fragmentation.

2018-01-24 | MSV000081963 | MassIVE

SNP analysis AID-low vs AID-high

Project description:SNP analysis AID-low vs AID-high

2009-07-20 | GSE13612 | GEO

Transcription profiling of mouse AID-GFP-positive vs AID-GFP-negative animals

Project description:Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative Experiment Overall Design: Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative

2009-08-22 | E-GEOD-13611 | biostudies-arrayexpress

Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative

Project description:Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative

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Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells.

Project description:Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells.

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Project description:Activation-induced cytidine deaminase (AID) specific amplifications and deletions in BCR-ABL1 positive Leukemia mouse cells. Bone marrow from Balb/CJ WT and Balb/CJ AID KO mice was transduced with BCR-ABL1. The AID specific amplifications and deletions where analyzed with an Agilent 244A mouse whole Genome CGH Array.

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