Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243644 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mice developed ovarian tumors after Arid1a and Pten double knockout. Gene expression profiles of 5 such ovarian tumors were compared with those of 4 normal ovaries. The differentially expressed genes were then used to investigate the similarity between the mouse ovarian tumors and major subtypes of human ovarian cancers. Total RNA obtained from the mouse ovarian tumors developing after Arid1a and Pten knockout compared to normal mouse ovaries.
2014-04-05 | E-GEOD-56531 | biostudies-arrayexpress
Project description:Prostate specific Pten deletion, Pten-Smad4 deletion, and Pten-p53 deletion
| PRJNA134477 | ENA
Project description:Prostate-specific Pten deletion and Pten-Lrf deletion
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Project description:Mice developed ovarian tumors after Arid1a and Pten double knockout. Gene expression profiles of 5 such ovarian tumors were compared with those of 4 normal ovaries. The differentially expressed genes were then used to investigate the similarity between the mouse ovarian tumors and major subtypes of human ovarian cancers.
2014-04-05 | GSE56531 | GEO
Project description:Acute Pten loss initiates prostate tumorigenesis characterized by cellular senescence response. Here we examine the cellular senescence response in epithelial individual cells, by single-cell RNA sequencing (scRNAseq) in Ptenpc-/- and Ptenpc-/-; Timp1-/- GEMMs. ScRNAseq analysis determines a cluster of senescent cells expressing the senescence-related genes. A significant positive correlation is observed between the senescence score and Bcl2 expression. This provides the rational for targeting senescent cells using Bcl2 inhibitor.
2020-10-09 | E-MTAB-9578 | biostudies-arrayexpress
Project description:KLF5 is a basic transcription factor that regulates multiple biological processes, but its function in tumorigenesis appears contradictory in the current literature, with some studies showing tumor suppressor activity and others showing tumor promoting activity. In this study, we examined the function of Klf5 in prostatic tumorigenesis using mice with prostate specific deletion of Klf5 and Pten, both of which are frequently deleted in human prostate cancer. Histological and molecular analyses demonstrated that when one Pten allele was deleted, which causes mouse intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth and caused more severe morphological and molecular alterations, and homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Klf5 deletion clearly promoted tumorigenesis in luminal cells, it actually diminished the numbers of Ck5-positive basal cells in the Pten-null tumors. Klf5 deletion also increased the cell proliferation rate in tumors with Pten deletion, which involved extensive activation of the PI3K/AKT and MAPK mitogenic signaling pathways and inactivation of the p15 cell cycle inhibitor. Global gene expression and pathway analyses demonstrated that multiple mechanisms could be responsible for the tumor promoting effect of Klf5 deletion, We used microarrays to detail the global programme of gene expression of Klf5-wildtype and Klf5-null mouse dorsal prostates under Pten-null context to figure out the differential expression profiling underlying tumorigenesis 4 Klf5-wildtype and 4 Klf5-null mouse (6 months age) dorsal prostates under Pten-null context were used for RNA extraction and hybridization on Affymetrix mouse st 1.0 array
2014-06-21 | E-GEOD-58719 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Genomewide analysis of PTEN deletion in mouse lung epithelial cells
| PRJNA205948 | ENA
Project description:Effects of Arid1a knockout in murine ovarian endometrioid carcinomas with biallelic inactivation of Apc and Pten
| PRJNA280703 | ENA
Project description:Coexistent ARID1A-PIK3CA mutations promote ovarian clear cell tumorigenesis through pro-tumorigenic inflammatory cytokine signaling
| PRJNA246369 | ENA