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Series GSE54313 Query DataSets for GSE54313
Status Public on Mar 19, 2014
Title Expression analysis of Mll3 knockdown p53-/- HSPC vs. control p53-/- HSPC
Organism Mus musculus
Experiment type Expression profiling by array
Summary Recurring deletions of chromosome 7 and 7q [-7/del(7q)] occur in myelodysplastic syndromes and acute myeloid leukemia (AML) and are associated with poor prognosis. However, the identity of specific tumor suppressors on 7q remains elusive. Using RNAi and CRISPR/Cas9 approaches, we show that a ~50% reduction in gene dosage of the mixed lineage leukemia 3 (MLL3) gene, located on 7q36.1, cooperates with other events occurring in -7/del(7q) AMLs to promote leukemogenesis. Mll3 suppression impairs the differentiation of HSPC. Interestingly, Mll3 suppressed leukemias, like human -7/del(7q) AMLs, are refractory to conventional chemotherapy but sensitive to the BET inhibitor JQ1. Thus, our mouse model functionally validates MLL3 as a haploinsufficient 7q tumor suppressor, and suggests a therapeutic option for this aggressive disease.
Overall design Total RNA obtained from sorted lin-ckit+ hematopoietic stem and progenitor cells of recipient mice transplanted with shRen;p53-/- or shMll3;p53-/- cells at 6 weeks after transplant
Contributor(s) Chen C, Liu Y, Lowe SW
Citation(s) 24794707
Submission date Jan 22, 2014
Last update date Jun 14, 2018
Contact name Chong Chen
Organization name Sichuan University
Department State Key Laboratory of Biotherapy
Lab Chong Chen
Street address 17 Renmin S. Road-No. 3
City Chengdu
State/province Sichuan
ZIP/Postal code 610041
Country China
Platforms (1)
GPL6885 Illumina MouseRef-8 v2.0 expression beadchip
Samples (8)
GSM1312822 shRen;p53-/- HSCPC Rep1
GSM1312823 shRen;p53-/- HSCPC Rep2
GSM1312824 shRen;p53-/- HSCPC Rep3
BioProject PRJNA236139

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Supplementary file Size Download File type/resource
GSE54313_RAW.tar 3.1 Mb (http)(custom) TAR
GSE54313_non_normalized.txt.gz 2.4 Mb (ftp)(http) TXT
Raw data are available on Series record
Processed data included within Sample table

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