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Series GSE6078 Query DataSets for GSE6078
Status Public on Nov 18, 2006
Title PTEN-deficient intestinal stem cells initiate intestinal polyposis
Organism Mus musculus
Experiment type Expression profiling by array
Summary Intestinal polyposis, a precancerous neoplasia, results primarily from an abnormal increase in the number of crypts. Crypts contain intestinal stem cells (ISCs). Thus intestinal polyposis provides an ideal condition for studying stem cell involvement in polyp/tumor formation. Using a conditional knock-out mouse model, we found that the tumor suppressor Phosphatase of Tension homolog (PTEN) governs the proliferation rate and number of ISCs and loss of PTEN results in an excess of ISCs. In PTEN mutants, excess ISCs initiate de-novo crypt formation and crypt fission, recapitulating crypt production in fetal/neonatal intestine. Microarray studies were used to profile the changes in gene expression that occurred when PTEN was knocked out in the intestine.
Keywords: Disease state analysis, genetic modification, Intestinal polyposis, PTEN mutant, Cowden disease mouse model
 
Overall design A conditional PTEN mutant allele [Groszer, M. et al. Negative regulation of neural stem/progenitor cell proliferation by the Pten tumor suppressor gene in vivo. Science 294, 2186-2189 (2001).] was combined with in interferon inducible Mx1-Cre [Kuhn, R., Schwenk, F., Aguet, M. & Rajewsky, K. Inducible gene targeting in mice. Science 269, 1427-1429 (1995).] to enable PTEN to be deleted from the intestine by administration of polyinosinic–polycytidylic acid (Poly I:C). PolyI:C was administered at weaning (every other day, five times total) to three PTEN mutant (Mx1-Cre positive:PTENfx/fx) and two control (Mx1-Cre negative:PTENfx/+) animals. Intestinal polyps (from PTEN mutants) and equivalent regions of intestine (from controls) were isolated 30 days after the final polyI:C injection. Microarray analysis compared the gene expression profiles of PTEN mutant polyps and control intestines. Genes were considered up-regulated or down-regulated if all of the following conditions were met: 1) There was at least a two-fold change in the average probe signal measured between controls and mutants; 2) There was no overlap between the range of mutant and control data; and 3) The control mean was outside the 95% confidence interval of the PTEN-mutant mean.
 
Contributor(s) He XC, Yin T, Grindley JC, Sato T, Hembree M, Wiedemann LM, Li L
Citation(s) 17237784
Submission date Oct 18, 2006
Last update date Feb 11, 2019
Contact name Linheng Li
E-mail(s) lil@stowers-institute.org
Phone 816-926-4081
URL http://www.stowers-institute.org
Organization name Stowers Institute for Medical Research
Street address 1000 East 50th Street
City Kansas City
State/province MO
ZIP/Postal code 64110
Country USA
 
Platforms (1)
GPL1261 [Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array
Samples (5)
GSM140792 Control_1_intestine_30days
GSM140813 PTEN_mutant_1_intestinal_polyp_30days
GSM140816 Control_2_intestine_30days
Relations
BioProject PRJNA97573

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Supplementary file Size Download File type/resource
GSE6078_RAW.tar 29.6 Mb (http)(custom) TAR (of CEL)
Raw data provided as supplementary file

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