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Series GSE48131 Query DataSets for GSE48131
Status Public on Jun 23, 2014
Title Ablation of Cdh1 and Trp53 in the uterus reveals novel mechanisms controlling tumor microenvironment in endometrial cancer.
Organism Mus musculus
Experiment type Expression profiling by array
Summary Because TP53 mutation and CDH1 inactivation are the most common abnormalities found in human type II endometrial carcinomas, the contribution of dysfunctional TRP53 and CDH1 in the tumor microenvironment to induce type II endometrial cancer was characterized using mouse as a model. The results of our analysis revealed that conditional deletion of Cdh1 and Trp53 in the uterus regulated most of the genes categorized by their involvement in inflammatory responses, immune cell trafficking, cellular movement, cell-to-cell signaling and interaction and cellular growth and proliferation.
 
Overall design A direct comparison of mouse uteri (n=3) from control, single ablation of Cdh1 or Trp53, and ablation of both Cdh1 and Trp53 at 2 months of age.
 
Contributor(s) Stodden GR, Lindberg ME, King ML, MacLean II JA, Hayashi K
Citation(s) 24998851
Submission date Jun 19, 2013
Last update date Jan 16, 2019
Contact name Kanako Hayashi
E-mail(s) k.hayashi@wsu.edu
Organization name Washington State University
Department School of Molecular Biosciences
Street address BLS345, 1770 NE Stadium Way
City Pullman
State/province WA
ZIP/Postal code 99164
Country USA
 
Platforms (1)
GPL6887 Illumina MouseWG-6 v2.0 expression beadchip
Samples (12)
GSM1169183 CO_1
GSM1169184 CO_2
GSM1169185 CO_3
Relations
BioProject PRJNA208971

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE48131_RAW.tar 15.8 Mb (http)(custom) TAR
GSE48131_non_normalized.txt.gz 6.3 Mb (ftp)(http) TXT
Processed data included within Sample table

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