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.
PTEN-deficient intestinal stem cells initiate intestinal polyposis.
No sample metadata fields
View SamplesLoss and heterozygosity for NDR1 predisposes mice to T-cell lymphoma development. To analyze mechanisms of tumor development in these mice chemically (ENU)-induced tumors were collected and RNA was extracted.
Ablation of the kinase NDR1 predisposes mice to the development of T cell lymphoma.
Sex, Specimen part, Disease, Treatment
View SamplesAffymetrix Human Gene 1.1 ST Array profiling of 285 primary medulloblastoma samples.
Subgroup-specific structural variation across 1,000 medulloblastoma genomes.
Sex, Age
View Samples