{"owner": "ArrayExpress Uploader", "pop_total": 0, "species": "mouse", "factors": [{"GSE16751GSM419953": {}}, {"GSE16751GSM419954": {}}, {"GSE16751GSM419955": {}}, {"GSE16751GSM419956": {}}, {"GSE16751GSM419957": {}}, {"GSE16751GSM419958": {}}], "id": 5739, "ownerprofile_id": "arrayexpress_sid", "platform": 6, "summary_wrapped": "Activation-Induced Cytidine Deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class switch recombination in...", "geo_gse_id": "E-GEOD-16751", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 0, "sample_count": 6, "tags": ["acute lymphoblastic leukemia", "bone", "bone marrow", "cell", "class", "immunoglobulin", "leukemia", "lymphoblastic leukemia"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_gds_id": "", "slug": "transcription-profiling-of-aid-expressing-leukemia", "geo_id_plat": "E-GEOD-16751_A-AFFY-45", "name": "Transcription profiling of AID expressing leukemia and AID deficient leukemia in a mouse model of BCR-ABL1 ALL", "created": "Nov.11, 2014", "summary": "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", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-16751", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-16751/samples/"}